2539 exam 2 metabolism, nutrition, perfusion, clotting

DIC lab and diagnostics

Results dropped in platelet count, an elevation in fibrin degradation products and D-dimer, an increase in PT and aPTT,low fibrinogen level ⬇️ Platelets ⬇️Fibrinogen ⬆️d-dimer ⬆️fibrin degradation product ⬆️PT; aPTT ⬆️Thrombin time

ventricular septal defect (VSD) manifestations

tiring easily, particularly with exertion or feeding. Failure to thrive color change or diaphoresis with nipple feeding in the infant frequent pulmonary infections shortness of breath edema mild tachypnea. holosystolic harsh murmur along the left sternal border. Adventitious lung sounds Palpate the chest for a thrill

HELLP: Diagnostic testing

A diagnosis of HELLP syndrome is made based on laboratory test results, including: Low hematocrit that is not explained by any blood loss Elevated LDH (liver impairment) Elevated AST (liver impairment) Elevated ALT (liver impairment) Elevated BUN Elevated bilirubin level Elevated uric acid and creatinine levels (renal involvement) Low platelet count (less than 100,000 cells/mm3)

Pancreatitis nursing care

* Pancreatitis patients put them in fetal position, NPO, gut rest, prepare antecubital site for PICC cuz they'll probably be getting TPN/Lipids Nursing Management Relieving Pain and Discomfort Because the pathologic process responsible for pain is Auto digestion of the pancreas, the objectives of therapy are to relieve pain and decrease secretion of pancreatic enzymes. The pain of acute pancreatitis is often very severe, necessitating the liberal use of analgesic agents. The current recommendation for pain management in this population is parenteral opioids, including morphine, hydromorphone, or fentanyl via patient-controlled analgesia or bolus (Marx et al., 2013). In critically ill patients, a continuous infusion may be needed. Because most opioids stimulate spasm of the sphincter of Oddi to some degree, consensus has not been reached on the most effective agent. Ensuring patient comfort, regardless of the opioid prescribed, is the most essential aspect of care. The nurse frequently assesses the pain and the effectiveness of the pharmacologic (and nonpharmacologic) interventions. Changes may be needed in the regimen for pain management based on the achievement of pain control. Pain assessment tools (see Chapter 12) are available for the nurse to ensure an accurate rating of pain. Nonpharmacologic interventions such as proper positioning, music, distraction, and imagery may be effective in reducing pain when used along with medications. In addition, oral feedings are withheld to decrease the secretion of secretin. Parenteral fluids and electrolytes are prescribed to restore And maintain fluid balance. Nasogastric suction may be used to relieve nausea and vomiting or to treat abdominal distention and paralytic ileus. The nurse provides frequent oral hygiene and care to decrease discomfort from the nasogastric tube and relieve dryness of the mouth. The acutely ill patient is maintained on bed rest to decrease the metabolic rate and reduce the secretion of pancreatic and gastric enzymes. If the patient experiences increasing severity of pain, the nurse reports this to the primary provider because the patient may be experiencing hemorrhage of the pancreas or the dose of analgesic medication may be inadequate. The patient with acute pancreatitis is often confused or delirious because of severe pain, fluid and electrolyte disturbances, and hypoxia. Therefore, the nurse provides frequent and repeated but simple explanations about the need for withholding fluids, maintenance of gastric suction, and bed rest. Improving Breathing Pattern The nurse maintains the patient in a semi-Fowler position to decrease pressure on the diaphragm by a distended abdomen and to increase respiratory expansion. Frequent changes of position are necessary to prevent atelectasis and pooling of respiratory secretions. Pulmonary assessment, including monitoring of pulse oximetry or arterial blood gases, is essential to detect changes in respiratory status so that early treatment can be initiated. The nurse instructs the patient in techniques of coughing and deep breathing and in the use of incentive spirometry to improve respiratory function and assists the patient to perform these activities every hour. Improving Nutritional Status The nurse assesses the patient's nutritional status and notes factors that alter the patient's nutritional requirements (e.g., temperature elevation, surgery, drainage). Laboratory test results and daily weights are useful to monitor the nutritional status. Enteral or parenteral nutrition may be prescribed. In addition to administering enteral or parenteral nutrition, the nurse monitors serum glucose levels every 4 to 6 hours. As the acute symptoms subside, oral feedings are gradually reintroduced. Between acute attacks, the patient receives a diet that is high in protein and low in fat (Dudek, 2013). The patient should avoid heavy meals and alcoholic beverages. Maintaining Skin Integrity The patient is at risk for skin breakdown because of poor nutritional status, enforced bed rest, and restlessness, which may result in pressure ulcers and breaks in tissue integrity. In addition, the patient who has undergone surgery may have multiple drains or an open surgical incision and is at risk for skin breakdown and infection. The nurse carefully assesses the wound, drainage sites, and skin for signs of infection, inflammation, and breakdown. The nurse carries out wound care as prescribed and takes precautions to protect intact skin from contact with drainage. Consultation with a wound-ostomy-continence (WOC) nurse, a nurse specially educated in appropriate skin, wound, ostomy, and continence care is often helpful in identifying appropriate skin care devices and protocols. The patient must be turned every 2 hours; the use of specialty beds may be indicated to prevent skin breakdown. Monitoring and Managing Potential Complications Fluid and electrolyte disturbances are common complications because of nausea, vomiting, movement of fluid from the vascular compartment to the peritoneal cavity, diaphoresis, fever, and the use of gastric suction. The nurse assesses the patient's fluid and electrolyte status by noting skin turgor and moistness of mucous membranes. The nurse weighs the patient daily and carefully measures fluid intake and output, including urine output, nasogastric secretions, and diarrhea. In addition, it is important to assess for other factors that may affect fluid and electrolyte status, including increased body temperature and wound drainage. The nurse assesses the patient for ascites and measures abdominal girth daily if ascites is suspected. Fluids are administered IV and may be accompanied by infusion of blood or blood products to maintain the blood volume and to prevent or treat hypovolemic shock. Emergency medications must be readily available because of the risk of circulatory collapse and shock. The nurse promptly reports decreased blood pressure and reduced urine output, which indicate hypovolemia and shock or acute kidney injury. Low serum calcium and magnesium levels may occur and require prompt treatment. Pancreatic necrosis is a major cause of morbidity and mortality in patients with acute pancreatitis because of resulting hemorrhage, septic shock, and MODS. The patient may undergo diagnostic procedures for confirmation of pancreatic necrosis. If the patient is found to have pancreatic necrosis with infection, this may require surgical, percutaneous or endoscopic débridement and/or insertion of multiple drains. Percutaneous or endoscopic catheter drainage is the first step of what is known as the "Step-Up Approach." Here, catheters are placed via the left or right retroperitoneal approach to drain the infection. This intervention, coupled with appropriate, targeted antibiotic therapy may be the only necessary treatment for some patients (da Costa, Boerma, van Santvoort, et al., 2014; Lankisch et al., 2015; Martin & Hein, 2013). These procedures are considered first-line approaches with surgery reserved for patients for whom these interventions do not work. Prophylactic antibiotics are not indicated (Lankisch et al., 2015; Zerem, 2014). The patient with pancreatic necrosis with or without infection is usually critically ill and requires expert medical and nursing management, including hemodynamic monitoring in the intensive care unit. In addition to carefully monitoring vital signs and other signs and symptoms, the nurse is responsible for administering prescribed fluids, medications, and blood products; assisting with supportive management, such as the use of a ventilator; preventing additional complications; and providing physical and psychological care. Shock and MODS may occur with acute pancreatitis. Hypovolemic shock may occur as a result of hypovolemia and sequestering of fluid in the peritoneal cavity. Hemorrhagic shock may occur with hemorrhagic pancreatitis. Septic shock may occur with bacterial infection of the pancreas. Cardiac dysfunction may occur as a result of fluid and electrolyte disturbances, acid-base imbalances, and release of toxic substances into the circulation. The nurse closely monitors the patient for early signs of neurologic, cardiovascular, renal, and respiratory dysfunction. The nurse must be prepared to respond quickly to rapid changes in the patient's status, treatments, and therapies. In addition, it is important to inform the family about the status and progress of the patient and to allow them to spend time with the patient. Management of shock and MODS is discussed in detail in Chapter 14.

ITP clinical manifestations

*Dry purpura -ecchymosis -petechiae -Simple bruising -easy bruising, heavy menses, and petechiae on the extremities or trunk *Wet purpura -epistaxia -menorrhagia -GI bleeding( mouth, pulmonary system) -hematuria - hemoptisis Platelet count often less than 30,000/mm3; less than 5000/mm3 is not uncommon. Common physical manifestations are easy bruising, heavy menses, and petechiae on the extremities or trunk Patients with simple bruising or petechiae ("dry purpura") tend to have fewer complications from bleeding than those with bleeding from mucosal surfaces, such as the GI tract (including the mouth) and pulmonary system (e.g., hemoptysis), which is termed wet purpura. Patients with wet purpura have a greater risk of life-threatening bleeding than do those with dry purpura; aggressive treatment should be promptly initiated. Severe thrombocytopenia (platelet count less than 20,000/mm3), a history of prior minor bleeding episodes, and advanced age also are predictive of severe bleeding (Arnold, 2015). Despite low platelet counts, the platelets are young and very functional. They adhere to endothelial surfaces and to one another, so spontaneous bleeding does not always occur. Thus, treatment may not be initiated unless bleeding becomes severe or life-threatening, or the platelet count is extremely low (less than 30,000/mm3)

Addison's disease manifestations

- Low blood pressure - Weakness and fatigue - Hyperpigmentation of mucous membranes and palms of hands muscle weakness; anorexia; GI symptoms; fatigue; emaciation; dark pigmentation of the mucous membranes and the skin, especially of the knuckles, knees, and elbows; hypotension; and low blood glucose, low serum sodium, and high serum potassium levels. Depression, emotional lability, apathy, and confusion are present in 20% to 40% of patients. pallor; complain of headache, abdominal pain, and diarrhea; and may show signs of confusion and restlessness. Even slight overexertion, exposure to cold, acute infection, or a decrease in salt intake may lead to circulatory collapse, shock, and death, if untreated.

Shock: General Management Strategies

- Supplemental O2 - Fluid replacement; table 14-3 - Vasoactive Meds (pg 296); disadvantage of meds is increased O2 demand from Heart - Calcium replacement Support of the respiratory system with supplemental oxygen and/or mechanical ventilation to provide optimal oxygenation (see Chapter 21) Fluid replacement to restore intravascular volume Vasoactive medications to restore vasomotor tone and improve cardiac function Nutritional support to address the metabolic requirements that are often dramatically increased in shock Therapies described in this section require collaboration among all members of the health care team pg.304 Vasoactive Medication Therapy Vasoactive medications are given in all forms of shock to improve the patient's hemodynamic stability when fluid therapy alone cannot maintain adequate MAP. Specific medications are selected to correct the particular hemodynamic alteration that is impeding cardiac output. These medications help increase the strength of myocardial contractility, regulate the heart rate, reduce myocardial resistance, and initiate vasoconstriction. Vasoactive medications are selected for their action on receptors of the sympathetic nervous system. These receptors are known as alpha-adrenergic and beta-adrenergic receptors. Beta-adrenergic receptors are further classified as beta-1 and beta-2 adrenergic receptors. When alpha-adrenergic receptors are stimulated, blood vessels constrict in the cardiorespiratory and GI systems, skin, and kidneys. When beta-1 adrenergic receptors are stimulated, heart rate and myocardial contraction increase. When beta-2 adrenergic receptors are stimulated, vasodilation occurs in the heart and skeletal muscles, and the bronchioles relax. The medications used in treating shock consist of various combinations of vasoactive medications to maximize tissue perfusion by stimulating or blocking the alpha- and beta-adrenergic receptors. When vasoactive medications are given, vital signs must be monitored frequently (at least every 15 minutes until stable, or more often if indicated). Vasoactive medications should be given through a central venous line, because infiltration and extravasation of some vasoactive medications can cause tissue necrosis and sloughing (Allen, 2014). Individual medication dosages are usually titrated by the nurse, who adjusts drip rates on the basis of the prescribed dose and target outcome parameter (e.g., BP, heart rate) and the patient's response. Dosages are changed to maintain the MAP at a physiologic level that ensures adequate tissue perfusion (usually greater than 65 mm Hg). Quality and Safety Nursing Alert Vasoactive medications should never be stopped abruptly, because this could cause severe hemodynamic instability, perpetuating the shock state. Dosages of vasoactive medications must be tapered. When vasoactive medications are no longer needed or are necessary to a lesser extent, the infusion should be weaned with frequent monitoring of BP (e.g., every 15 minutes). Table 14-2 presents some of the commonly prescribed vasoactive medications used in the treatment of shock. Occasionally, the patient does not respond as expected to vasoactive medications. A current topic of active research is evaluation of patients' adrenal function. Recent studies suggest that critically ill patients should be evaluated for corticosteroid insufficiency (also referred to as relative adrenal insufficiency or critical illness-related corticosteroid insufficiency) and, if this condition is present, corticosteroid replacement (e.g., hydrocortisone) should be considered (Dellinger et al., 2013)

Abdominal Aortic Aneurysm signs and symptoms

-Abdominal pain radiating to the back - if AAA is large enough, it can be felt pulsating. -may reveal absent pulse in extremities Abdominal Aortic Aneurysm s/s Some patients complain that they can feel their heart beating in their abdomen when lying down, or they may say that they feel an abdominal mass or abdominal throbbing. If the abdominal aortic aneurysm is associated with thrombus, a major vessel may be occluded or smaller distal occlusions may result from emboli. Small cholesterol, platelet, or fibrin emboli may lodge in the interosseous or digital arteries, causing cyanosis and mottling of the toes. Signs of impending rupture include severe back or abdominal pain, which may be persistent or intermittent. Abdominal pain is often localized in the middle or lower abdomen to the left of the midline. Low back pain may be present because of pressure of the aneurysm on the lumbar nerves. Indications of a rupturing abdominal aortic aneurysm include constant, intense back pain; falling blood pressure; and decreasing hematocrit A retroperitoneal rupture of an aneurysm may result in hematomas in the scrotum, perineum, flank, or penis. Signs of heart failure or a loud bruit may suggest a rupture into the vena cava. The high blood pressure and increased blood volume returning to the right side of the heart from the vena cava may cause right-sided heart failure

Atrial Flutter Treatment

-Give anticoagulants (faster the HR, more risk for thrombus) -treat underlying cause -digoxin (slows rate by enhancing AV block) -Quinidine (supresses atrial ectopic block) -Amiodarone -Calcium Channel Blockers (Cardizem)/Beta Blockers (-olol) -consider cardio version Atrial flutter occurs because of a conduction defect in the atrium and causes a rapid, regular atrial impulse at a rate between 250 and 400 bpm. Because the atrial rate is faster than the AV node can conduct, not all atrial impulses are conducted into the ventricle, causing a therapeutic block at the AV node. This is an important feature of this dysrhythmia. If all atrial impulses were conducted to the ventricle, the ventricular rate would also be 250 to 400 bpm, which would result in ventricular fibrillation, a life-threatening dysrhythmia. Atrial flutter risk factors mirror those for atrial fibrillation Atrial flutter has the following characteristics: Ventricular and atrial rate: Atrial rate ranges between 250 and 400 bpm; ventricular rate usually ranges between 75 and 150 bpm. Ventricular and atrial rhythm: The atrial rhythm is regular; the ventricular rhythm is usually regular but may be irregular because of a change in the AV conduction. QRS shape and duration: Usually normal, but may be abnormal or may be absent. P wave: Saw-toothed shape; these waves are referred to as F waves. PR interval: Multiple F waves may make it difficult to determine the PR interval. P:QRS ratio: 2:1, 3:1, or 4:1 Medical Management Atrial flutter can cause serious signs and symptoms, such as chest pain, shortness of breath, and low blood pressure. Medical management involves the use of vagal maneuvers or a trial administration of adenosine, which causes sympathetic block and slowing of conduction through the AV node. This may terminate the tachycardia; optimally, it will facilitate visualization of flutter waves for diagnostic purposes. Adenosine is given intravenously by rapid administration, and immediately followed by a 20-mL saline flush and elevation of the arm with the IV line to promote rapid circulation of the medication. Atrial flutter is treated with antithrombotic therapy, rate control, and rhythm control in the same manner as atrial fibrillation. Electrical cardioversion is often successful in converting atrial flutter to sinus rhythm

Pancreatitis clinical manifestations

-Initially,- severe abd pain, midepigastrium, distention, N/V, Pain is frequently acute in onset, occurring 24 to 48 hours after a very heavy meal or alcohol ingestion, and it may be diffuse and difficult to localize. It is generally more severe after meals and is unrelieved by antacids -As pancreatitis continues- rigid abdomen, bruising around umbilicus, bile stained emesis, fever, jaundice, mental confusion -Hypovolemia, hypotension, acute renal failure, respiratory distress may also occur.

stages of shock and SS

1. agitation, restlessness; increased HR, cool clammy skin 2. confusion, CPP, CO, SBP low. HR up, oliguria 3. edema, hypotension, dysrhythmia, weak thready pulse, cold clammy skin 4. hypotension, HR slow, MODS< hypoxemia, acidosis. not respond to vasopressor Compensatory: BP:Normal HR:>100 RR:>20 PCO2<32 Skin:cold clammy Urinary output: decreased Mentation:confusion and or agitation Acid base balance: respiratory alkalosis Progressive: BP:systolic <90. MAP <65 HR:>150 RR:rapid shallow respiration's crackles PaO2<80 PaCO2 >45 Skin:mothed petechiae Urinary output: < 0.5 ml Mentation:lethargy Acid base balance:metabolic acidosis Irreversible: BP: requires mechanical or pharmacological support HR: erratic RR: requires intubation and mechanical ventilation and oxygen Skin: jaundice Urinary output: anuric, requires dialysis Mentation: unconscious Acid base balance profound acidosis

failure to thrive risk factors

-Low birth weight -Living in poverty -Foster care -Physical or mental disability -Caretaker neglect Failure to thrive (FTT) is a term used to describe inadequate growth in infants and children. The child fails to demonstrate appropriate weight gain over a prolonged period of time. Length or height velocity and head circumference growth may also be affected. Typical children may experience FTT, but it is much more common in the child with special needs. Adequate nutrition is critical for appropriate brain growth in the first 2 years of life and obviously for growth in general throughout childhood and adolescence (Starr et al., 2013). FTT is a multifactorial problem. Developmental disability (mental or physical or combination impairment resulting in lifelong disability) may contribute to FTT, as the child's ability to consume adequate nutrition is impaired because of sensory or motor delays, such as with cerebral palsy. Other organic causes of FTT include inability to suck and/or swallow correctly, malabsorption, diarrhea, vomiting, or alterations in metabolism and caloric/nutrient needs associated with a variety of chronic illnesses. Infants and children with cardiac or metabolic disease, chronic lung disease (bronchopulmonary dysplasia), cleft palate, or gastroesophageal reflux disease are at particular risk. Feeding disorders or food refusal may occur in infants or children who have required prolonged mechanical ventilation, long-term enteral tube feedings, or an unpleasant event such as a choking episode. Additional causes of FTT include neglect, abuse, behavioral problems, lack of appropriate maternal interaction, poor feeding techniques, lack of parental knowledge, or parental mental illness. Poverty is the single greatest contributing risk factor (Kirkland & Motil, 2015a; Starr et al., 2013). Screen all children for FTT to identify them early. In addition to poor growth, the infant or child with FTT may present with a history of developmental delay or loss of acquired milestones. Infants or children with feeding problems may display nipple, spoon, or food refusal; difficulty sucking; disinterest in feeding; or difficulty progressing from liquid to purée to texture food. Perform a detailed dietary history and instruct the parents to complete a 3-day food diary to identify what the child actually eats and drinks. Assess the parent-child interaction, with particular attention to the parent's ability to read and respond to the infant's or child's cues. Observe feeding, noting the child's oral interest or aversion, oral-motor coordination, and swallowing ability, as well as parent-child interactions before, during, and after the feeding.

HIT medical managements/Pharmacological and Parenteral Therapies Adverse Outcomes

-NO heparin!! -may start w/ coumadin w/ platelets > 150,000 -plasmapheresis -protamine sulfate IV -thrombin inhibitors: decrease coagulation process Affected patients are at increased risk for thrombosis, either venous, arterial, or both, and the thrombosis can range from DVT to ACS or stroke, or to ischemic damage to an extremity, necessitating amputation. VTE is the most common, typically DVT or PE (Lee & Arepally, 2013). Treatment for HIT includes prompt cessation of heparin (including any heparin-coated catheters) and initiation of an alternative means of anticoagulation. If the heparin is stopped without providing additional anticoagulation, the patient is at increased risk for developing new thrombi. Argatroban is an inhibitor of thrombin and an FDA-approved anticoagulant for the treatment of HIT. Oral anticoagulation with warfarin is contraindicated because it initially promotes thrombosis in the microvasculature by depleting protein C, which can lead to ischemia and gangrenous limbs (Greinacher, 2015). Once the platelet count has recovered, transitioning to treatment with warfarin is possible. Individuals who develop thrombosis in the setting of HIT should receive anticoagulation for 3 to 6 months; the duration of anticoagulation in the absence of thrombosis is shorter (Lee & Arepally, 2013). Patients need to be aware of their risk for reactivation Of the disorder should they be exposed to any amount of heparin within 3 to 4 months after diagnosis. This time frame is thought to be sufficient to remove anti-heparin-platelet antibodies from the circulation by the RES.

blood transfusion process

-Verify order & obtain consent -type & cross-match blood sample -Large bore catheter: 18g & administer with isotonic saline -Baseline vitals, hold & notify if abnormal -Pre-medication may be ordered: benadryl or tylenol -DOUBLE CHECK with TWO RNs at patient's bedside: everything must match -Begin transfusion slowly, observe for 15 mins, stop if any sign of reaction -Blood may not hang longer than 4 hours

MI treatment guidelines

1) *Morphine* 2-4mg IV (pain + vasodilator - removes vasospasm around the infarction) - dark ecplisde = numbra - light = penumbra (area around thrombosed vessel is little spasming vessels) - *reverses ischemia penumbra* 2) *O2* - 100% non re breather (unless COPD) 3) *Nitroglycerin* (CA dilator) - IV 10-200micrograms/min, or sublingual 4) *Aspirin* - 325mg immediately + *ANGIOPLASTY* (open vessel within an hour!) - put a stent in cath lab - *ACE inhibitors* decrease afterload - *atenolol* (or other beta blocker) - *tPA* (esp if you don't have a cath lab available) - CI (high BP, bleeding diathesis, brain tumor or something) Treatment Guidelines for Acute Myocardial Infarction Use rapid transit to the hospital. Obtain 12-lead electrocardiogram to be read within 10 minutes. Obtain laboratory blood specimens of cardiac biomarkers, including troponin. Obtain other diagnostics to clarify the diagnosis. Begin routine medical interventions: Supplemental oxygen Nitroglycerin Morphine Aspirin Beta-blocker Angiotensin-converting enzyme inhibitor within 36 hours Anticoagulation with heparin and platelet inhibitors Statin Evaluate for indications for reperfusion therapy: Percutaneous coronary intervention Thrombolytic (fibrinolytic) therapy Continue therapy as indicated: IV heparin, low-molecular-weight heparin, bivalirudin, or fondaparinux Clopidogrel (Plavix) Glycoprotein IIb/IIIa inhibitor Bed rest for a minimum of 12-24 hours Statin prescribed at discharge.

ventricular fibrillation treatment

ACLS Un-Sync. Cardioversion Followed by IV Amiodarone or epinephrine The most common dysrhythmia in patients with cardiac arrest is ventricular fibrillation, which is a rapid, disorganized ventricular rhythm that causes ineffective quivering of the ventricles. No atrial activity is seen on the ECG. The most common cause of ventricular fibrillation is coronary artery disease and resulting acute MI. Other causes include untreated or unsuccessfully treated VT, cardiomyopathy, valvular heart disease, several proarrhythmic medications, acid-base and electrolyte abnormalities, and electrical shock. Another cause is Brugada syndrome, in which the patient (frequently of Asian descent) has a structurally normal heart, few or no risk factors for coronary artery disease, and a family history of sudden cardiac death (Aizawa, Takatsuki, Sano, et al., 2013; Tokioka, Kusano, Morita, et al., 2014). Ventricular fibrillation has the following characteristics (see Fig. 26-17): Characteristics: QRS shape and duration: Irregular, undulating waves with changing amplitudes. There are no recognizable QRS complexes Medical Management Ventricular fibrillation is always characterized by the absence of an audible heartbeat, a palpable pulse, and respirations. Because there is no coordinated cardiac activity, cardiac arrest and death are imminent if the dysrhythmia is not corrected. Early defibrillation is critical to survival, with administration of immediate bystander cardiopulmonary resuscitation (CPR) until defibrillation is available. For refractory ventricular fibrillation, administration of amiodarone and epinephrine may facilitate the return of a spontaneous pulse after defibrillation (Link et al., 2015) (see Chapter 29 for further discussion on interventions during Cardiac Arrest).

Coarctation of Aorta treatment

Balloon angioplasty until lesion can be surgically corrected.then stent or anastomosis after resection catheterization is possible in some children. • Most common surgical repair is resection of the narrowed portion of the aorta, followed by end-to-end reanastomosis. • Preoperatively, administer prostaglandin medications as ordered to relax the ductal tissue. • Postoperatively, measure and compare BP in all four extremities and quality of upper vs. lower pulses Signs: systolic murmur, hypertension, diminished femoral pulses Diagnosis: echocardiography Treatment: pre-op prostaglandins to reopen ductus arteriosus + surgical repair

DIC signs and symptoms

Bleeding gums or nose; reduced lab values for platelets, fibrinogen, bleeding from injection sites, IV sites; ecchymosis Possible signs of bleeding into the skin, such as cutaneous oozing, petechiae, ecchymosis, and hematomas. -Possible bleeding from surgical or invasive procedural sites, such as incisions an venipuncture sites. -Possible GI bleeding and hematuria -Purpura, jaundice -Hemoptysis (coughing up blood) -epistaxis (nose bleed) -seizures -oliguria -acrocyanosis (bluish or purplish color of the hands and feet caused by slowed circulation) -Dyspnea or tachypnea -Mental status changes, including confusioN

MI cardiac Rehabilitation

Cardiac Rehabilitation After the patient with an MI is in a stable condition, an active rehabilitation program is initiated. Cardiac rehabilitation is an important continuing care program for patients with CAD that targets risk reduction by providing patient and family education, offering individual and group support, and encouraging physical activity and physical conditioning. The goals of rehabilitation for the patient who has had an MI are to extend life and improve the quality of life. The immediate objectives are to limit the effects and progression of atherosclerosis, return the patient to work and a pre-illness lifestyle, enhance the patient's psychosocial and vocational status, and prevent another cardiac event. Cardiac rehabilitation programs increase survival, reduce recurrent events and the need for interventional procedures, and improve quality of life (Amsterdam et al., 2014). Physical conditioning is achieved gradually over time. Many times, patients will "overdo it" in an attempt to achieve their goals too rapidly. Patients are observed for chest pain, dyspnea, weakness, fatigue, and palpitations and are instructed to stop exercise if any of these occur. Patients may also be monitored for an increase in heart rate above the target heart rate, an increase in systolic or diastolic blood pressure of more than 20 mm Hg, a decrease in systolic blood pressure, onset or worsening of dysrhythmias, or ST-segment changes on the ECG. Cardiac rehabilitation programs are categorized into three phases (Fletcher, Ades, Kligfield, et al., 2013). Phase I begins with the diagnosis of atherosclerosis, which may occur when the patient is admitted to the hospital for ACS. Because of brief hospital lengths of stay, mobilization occurs early and patient education focuses on the essentials of self-care rather than instituting behavioral changes for risk reduction. Priorities for in-hospital education include the signs and symptoms that indicate the need to call 911 (seek emergency assistance), the medication regimen, rest-activity balance, and follow-up appointments with the primary provider. The patient is reassured that although CAD is a lifelong disease and must be treated as such, he or she can likely resume a normal life after an MI. The amount and type of activity recommended at discharge depend on the patient's age, his or her condition before the cardiac event, the extent of the disease, the course of the hospital stay, and the development of any complications. Phase II occurs after the patient has been discharged. The patient attends sessions three times a week for 4 to 6 weeks but may continue for as long as 6 months. The outpatient program consists of supervised, often ECG-monitored, exercise training that is individualized. At each session, the patient is assessed for the effectiveness of and adherence to the treatment. To prevent complications and another hospitalization, the cardiac rehabilitation staff alerts the referring primary provider to any problems. Phase II cardiac rehabilitation also includes educational sessions for patients and families that are given by cardiologists, exercise physiologists, dietitians, nurses, and other health care professionals. These sessions may take place outside a traditional classroom setting. For instance, a dietitian may take a group of patients to a grocery store to examine labels and meat selections or to a restaurant to discuss menu offerings for a heart-healthy diet. Phase III is a long-term outpatient program that focuses on maintaining cardiovascular stability and long-term conditioning. The patient is usually self-directed during this phase and does not require a supervised program, although it may be offered. The goals of each phase build on the accomplishments of the previous phase.

MI Health promotion

Chart 27-10 HEALTH PROMOTION Promoting Health After Myocardial Infarction and Other Acute Coronary Syndromes To extend and improve the quality of life, a patient who has had a myocardial infarction (MI) must make lifestyle adjustments to promote heart-healthy living. With this in mind, the nurse and patient develop a program to help achieve desired outcomes. Making Lifestyle Modifications During Convalescence and Healing Adaptation to an MI is an ongoing process and usually requires some modification of lifestyle. Educate patients to make the following specific modifications: Avoid any activity that produces chest pain, extreme dyspnea, or undue fatigue. Avoid extremes of heat and cold and walking against the wind. Lose weight, if indicated. Stop smoking and the use of tobacco; avoid secondhand smoke. Develop heart-healthy eating patterns, and avoid large meals and hurrying while eating. Modify meals to align with the Therapeutic Lifestyle Changes (TLC) or other recommended diets. Adhere to medical regimen, especially in taking medications. Follow recommendations that ensure that blood pressure and blood glucose are in control. Pursue activities that relieve and reduce stress. Adopting an Activity Program In addition, the patient needs to undertake a structured program of activity and exercise for long-term rehabilitation. Advise patients to: Engage in a regimen of physical conditioning with a gradual increase in activity duration and then a gradual increase in activity intensity. Enroll in a cardiac rehabilitation program. Walk daily, increasing distance and time as prescribed. Monitor pulse rate during physical activity. Avoid physical exercise immediately after a meal. Alternate activity with rest periods (some fatigue is normal and expected during convalescence). Participate in a daily program of exercise that develops into a program of regular exercise for a lifetime. Managing Symptoms The patient must learn to recognize and take appropriate action for recurrent symptoms. Make sure that patients know to do the following: Call 911 if chest pressure or pain (or prodromal symptoms) is not relieved in 15 minutes by taking 3 nitroglycerin tablets at 5-minute intervals. Contact the primary provider if any of the following occur: shortness of breath, fainting, slow or rapid heartbeat, swelling of feet and ankles.

MI treatment guidelines pharmacological

Chart 27-8 PHARMACOLOGY Administration of Thrombolytic (Fibrinolytic) Therapy Indications Chest pain lasting more than 20 minutes, unrelieved by nitroglycerin ST-segment elevation in at least two leads that face the same area of the heart Less than 6 hours from onset of pain Absolute Contraindications Active bleeding Known bleeding disorder History of hemorrhagic stroke History of intracranial vessel malformation Recent major surgery or trauma Uncontrolled hypertension Pregnancy Nursing Considerations Minimize the number of times the patient's skin is punctured. Avoid intramuscular injections. Draw blood for laboratory tests when starting the IV line. Start IV lines before thrombolytic (fibrinolytic) therapy; designate one line to use for blood draws. Avoid continual use of noninvasive blood pressure cuff. Monitor for acute dysrhythmias and hypotension. Monitor for reperfusion: resolution of angina or acute ST-segment changes. Check for signs and symptoms of bleeding: decrease in hematocrit and hemoglobin values, decrease in blood pressure, increase in heart rate, oozing or bulging at invasive procedure sites, back pain, muscle weakness, changes in level of consciousness, complaints of headache. Treat major bleeding by discontinuing thrombolytic (fibrinolytic) therapy and any anticoagulants; apply direct pressure and notify the primary provider immediately. Treat minor bleeding by applying direct pressure if accessible and appropriate; continue to monitor.

Myocardial Infarction Percutanous Transluminal Coronary Angioplasty/potential for complications of treatment

Complications that can occur during a PCI procedure include coronary artery dissection, perforation, abrupt closure, or vasospasm. Additional complications include acute MI, serious dysrhythmias (e.g., ventricular tachycardia), and cardiac arrest. Some of these complications may require emergency surgical treatment. Complications after the procedure may include abrupt closure of the coronary artery and a variety of vascular complications, such as bleeding at the insertion site, retroperitoneal bleeding, hematoma, and arterial occlusion (Douglas & Applegate, 2013). In addition, there is a risk of acute kidney injury from the contrast agent used during the procedure (see Table 27-4)

patent ductus arteriosus signs and symptoms

Continuous, rumbling, machine-like murmur (2nd intercostal space at LUSB) Bounding pulses frequent respiratory infections fatigue poor growth and development tachycardia tachypnea bounding peripheral pulses widened pulse pressure. The diastolic BP typically is low due to the shunting. ****Auscultate the lungs and heart, noting rales if heart failure is present. Note a harsh, continuous, machine-like murmur, usually loudest under the left clavicle at the first and second intercostal spaces*** The nurse is caring for a term neonate who is diagnosed with patent ductus arteriosus. While performing a physical assessment of the neonate, the nurse anticipates that the neonate will exhibit which signs? Loud cardiac murmurs through systole and diastol When assessing a neonate who was born at 30 weeks' gestation, a nurse notes bounding femoral pulses, a palpable thrill over the suprasternal notch, tachycardia, tachypnea, and crackles. The nurse suspects: Patent ductus arteriosu

TOF: Hypercyanotic spells

Determine if the infant or child is demonstrating hypercyanotic spells. Hypercyanosis develops suddenly and is manifested as increased cyanosis, hypoxemia, dyspnea, and agitation. If the infant's oxygen demand is greater than the supply, such as with crying or during feeding, then the spell progresses to anoxia. When the degree of cyanosis is severe and persistent, the infant may become unresponsive. As the infant gets older, he or she may use specific postures, such as bending at the knees or assuming the fetal position, to relieve a hypercyanotic spell. The walking infant or toddler may squat periodically. These positions improve pulmonary blood flow by increasing systemic vascular resistance. Ask the parents if they have noticed any of these unusual positions. Note history of irritability, sleepiness, or difficulty breathing RELIEVING HYPERCYANOTIC SPELLS Use a calm, comforting approach. Place the infant or child in a knee-to-chest position. Provide supplemental oxygen. Administer morphine sulfate (0.1 mg/kg IV, IM, or SQ). Supply IV fluids. Administer propranolol (0.1 mg/kg IV). A child diagnosed with tetralogy of Fallot becomes upset, cries, and thrashes around when a blood specimen is obtained. The child becomes cyanotic and the respiratory rate increases to 44 breaths/min. Which action should the nurse do first? Place the child in a knee-to-chest position

Hypovolemic shock causes

Hemorrhage, Vomiting and Diarrhea, Dehydration, Third-space loss, Burns Hypovolemic shock can be caused by external fluid losses, as in traumatic blood loss, or by internal fluid shifts, as in severe dehydration, severe edema, or ascites (see Chart 14-3) Hypovolemic Shock External: Fluid Losses Trauma Surgery Vomiting Diarrhea Diuretics Diabetes insípidus Internal: Fluid Shift Hemorrhage Burns Ascites Peritonitis Dehydration Necrotizing pancreatitis

ventricular septal defect (VSD) treatment

If surgical closure is required, it should be performed before permanent pulmonary vascular changes develop. • Surgical closure may be in the form of suture closure of the VSD, transcatheter placement of a device in the defect, or Dacron patch closure. • Monitor for ventricular dysrhythmias or AV block. • With the clamshell occluding or Amplatzer device, strenuous activity should be avoided for 1 month after the procedure. Oxygen supplementation is not helpful.

patent ductus arteriosus (PDA) treatment

Indomethacin (blocks PGE synthesis) • PDA is closed by coil embolization or device via cardiac catheterization. • May also be surgically ligated.

coartation of the aorta signs and symptoms

Infantile type - aortic stenosis proximal to insertion of ductus arteriosis (preductal) Adult type - stenosis is distal to ductus arteriosus (postductal). Associated with notching of ribs (due to collateral circ), HTN in upper extremities, weak pulses in lower, assoc with Turner's, can cause aortic regurgitation problems with irritability and frequent epistaxis. In older children, there also may be reports of leg pain with activity, dizziness, fainting, and headaches. Assess pulses throughout, noting full, bounding pulses in the upper extremities with weak or absent pulses in the lower extremities. Determine BP in all four extremities. BP in the upper extremities may be 20 mm Hg or higher than that in the lower extremities. Inspect the school-age child's chest, noting notching of the ribs. Auscultate the heart for a soft or moderately loud systolic murmur, most often heard at the base of the heart (on the back or in the left axilla) (Darst et al., 2014) Assessment of a term neonate at 8 hours after birth reveals tachypnea, diminished femoral pulses, and poor lower body perfusion. The nurse notifies the health care provider (HCP) based on the interpretation that these symptoms are associated with which complication? Coarctation of the aort A child, age 4, is admitted with a tentative diagnosis of congenital heart disease. When assessment reveals a bounding radial pulse coupled with a weak femoral pulse, the nurse suspects that the child has: Coarctation of the aorta

Pacemakers: Complications

Infection Bleeding or Hematoma Formation Dislocation of lead Skeletal muscle or phrenic nerve stimulation Cardiac Tamponade Pacemaker malfunction Potential Complications from Insertion of a Pacemaker Local infection at the entry site of the leads for temporary pacing, or at the subcutaneous site for permanent generator placement. Prophylactic antibiotic and antibiotic irrigation of the subcutaneous pocket prior to generator placement has decreased the rate of infection to a minimal rate. Pneumothorax; the use of sheaths marketed as "safe" reduces this risk. Bleeding and hematoma at the lead entry sites for temporary pacing, or at the subcutaneous site for permanent generator placement. This usually can be managed with cold compresses and discontinuation of antiplatelet and antithrombotic medications. Hemothorax from puncture of the subclavian vein or internal mammary artery. Ventricular ectopy and tachycardia from irritation of the ventricular wall by the endocardial electrode. Movement or dislocation of the lead placed transvenously (perforation of the myocardium). Phrenic nerve, diaphragmatic (hiccuping may be a sign), or skeletal muscle stimulation if the lead is dislocated or if the delivered energy (mA) is set high. The occurrence of this complication is avoided by testing during device implantation. Cardiac perforation resulting in pericardial effusion and, rarely, cardiac tamponade, which may occur at the time of implantation or months later. This condition can be recognized by the change in QRS complex morphology, diaphragmatic stimulation, or hemodynamic instability. Twiddler syndrome may occur when the patient manipulates the generator, causing lead dislodgement or fracture of the lead. Pacemaker syndrome (hemodynamic instability caused by ventricular pacing and the loss of AV synchrony)

Addison's disease/ addisonian crisis

Manifestations= hypotension, cyanosis, fever, nausea, vomiting, and signs of shock) Monitoring and Managing Addisonian Crisis The patient at risk is monitored for signs and symptoms indicative of addisonian crisis, which can include shock; hypotension; rapid, weak pulse; rapid respiratory rate; pallor; and extreme weakness .Physical and psychological stressors such as cold exposure, overexertion, infection, and emotional distress should be avoided. The patient with addisonian crisis requires immediate treatment with IV administration of fluid, glucose, electrolytes, especially sodium, replacement of missing steroid hormones; and vasopressors. The nurse anticipates and meets the patient's needs to promote return to a precrisis state. Restoring Fluid Balance The nurse encourages the patient to consume foods and fluids that assist in restoring and maintaining fluid and electrolyte balance. Along with the dietitian, the nurse helps the patient select foods high in sodium during GI disturbances and in very hot weather. The nurse educates the patient and family to administer hormone replacement as prescribed and to modify the dosage during illness and other stressful situations. Written and verbal instructions are provided about the administration of corticosteroids (hydrocortisone, cortisone, and prednisone) and mineralocorticoids (fludrocortisone [Florinef]) as prescribed. Improving Activity Tolerance Until the patient's condition is stabilized, the nurse takes precautions to avoid unnecessary activity and stress that could precipitate another hypotensive episode. Efforts are made to detect signs of infection or the presence of other stressors. Explaining the rationale for minimizing stress during the acute crisis assists the patient to increase activity gradually.

Atrial Fibrillation (A-Fib) medical management treatment

Medical management revolves around preventing embolic events such as stroke with antithrombotic drugs, controlling the ventricular rate of response with antiarrhythmic agents, and treating the dysrhythmia as indicated so that it is converted to a sinus rhythm (i.e., cardioversion). Antithrombotic Medications. Antithrombotic drugs may include anticoagulants and antiplatelet drugs Medications That Control the Heart Rate. A strategy to control the ventricular rate of response so that the resting heart rate is less than 80 bpm is recommended in order to manage symptoms of atrial fibrillation. To decrease the ventricular rate in patients with paroxysmal, persistent, or permanent atrial fibrillation, a beta-blocker or non-dihydropyridine calcium channel blockers is generally recommended. Medications That Convert the Heart Rhythm or Prevent Atrial Fibrillation. For patients with atrial fibrillation lasting 48 hours or longer, anticoagulation is recommended prior to attempts to restore sinus rhythm, which may be achieved through pharmacological or electrical cardioversion. In the absence of therapeutic anticoagulation, TEE may be performed prior to cardioversion to identify left atrial thrombus formation, including in the LAA.If no thrombus is identified, cardioversion can proceed. Medications that may be given to achieve pharmacologic cardioversion to sinus rhythm include flecainide (Tambocor), dofetilide (Tikosyn), propafenone (Rythmol), amiodarone, and IV ibutilide (Corvert). These medications are most effective if given within 7 days of the onset of atrial fibrillation. It is recommended that patients who were prescribed dofetilide be hospitalized so that the QT interval and renal function both may be monitored. Despite a degree of risk, dofetilide is a preferred medication because it is highly effective at converting atrial fibrillation to sinus rhythm, has fewer drug-to-drug interactions, and is better tolerated by patients than other medications. Some patients with recurrent atrial fibrillation may be prescribed flecainide to self-administer at home, an approach referred to as "pill in the pocket" (January et al., 2014). Prevention of atrial fibrillation following cardiac surgery is best achieved through administration of beta-blockers for at least 24 hours prior to surgery (Shi, 2016). Cholesterol-lowering drugs such as the HMG-CoA reductase inhibitors (also called "statins," see Chapter 27, Table 27-2) may also be prescribed for primary prevention of new-onset atrial fibrillation following cardiac surgery. Therapy with angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) may decrease the incidence of atrial fibrillation for patients with concomitant hypertension, although the use of these drugs is not found to be beneficial as a primary prevention strategy for patients without hypertension. If symptomatic, paroxysmal atrial fibrillation is refractory to at least one Class I or Class III antiarrhythmic medication, and rhythm control is desired, catheter ablation may be indicated. Electrical Cardioversion for Atrial Fibrillation Electrical cardioversion is indicated for patients with atrial fibrillation that is hemodynamically unstable (e.g., acute alteration in mental status, chest discomfort, hypotension) and does not respond to medications . Flecainide, propafenone, amiodarone, dofetilide, or sotalol may be given prior to cardioversion to enhance the success of cardioversion and maintain sinus rhythm. Because atrial function may be impaired for several weeks after cardioversion, warfarin is indicated for at least 4 weeks after the procedure. Repeated attempts at electrical cardioversion may be made, following administration of an anti arrhythmic medication.

Cushing's disease diagnostic testing

Metabolism/Cushing Disease/Diagnostic Assessment and Diagnostic Findings The three tests used to diagnose Cushing syndrome are serum cortisol, urinary cortisol, and low-dose dexamethasone (Decadron) suppression tests (Nieman, 2016d). Two of these three tests need to be unequivocally abnormal to diagnose Cushing syndrome. If the results of all three tests are normal, the patient likely does not have Cushing syndrome (but may have a mild case, or the manifestations may be cyclic). For these patients, further testing is not recommended unless symptoms progress. If test results are either slightly abnormal or discordant, further testing is recommended. Serum cortisol levels are usually higher in the early morning (6 to 8 am) and lower in the evening (4 to 6 pm). This variation is lost in patients with Cushing syndrome (Fischbach & Dunning, 2015). A urinary cortisol test requires a 24-hour urine collection. The nurse instructs the patient how to collect and store the specimen. If the results of the urinary cortisol test are three times the upper limit of the normal range and one other test is abnormal, Cushing syndrome can be assumed. An overnight dexamethasone suppression test is used to diagnosis pituitary and adrenal causes of Cushing syndrome. It can be performed on an outpatient basis. Dexamethasone (1 mg or 8 mg) is given orally late in the evening or at bedtime, and a plasma cortisol level is obtained at 8 am the next morning. Suppression of cortisol to less than 5 mg/dL indicates that the hypothalamic-pituitary-adrenal axis is functioning properly (Fischbach & Dunning, 2015). Stress, obesity, depression, and medications such as anticonvulsant agents, estrogen (during pregnancy or as oral medications), and rifampin (Rifadin) can falsely elevate cortisol levels. Indicators of Cushing syndrome include an increase in serum sodium and blood glucose levels and a decrease in serum potassium, a reduction in the number of blood eosinophils, and disappearance of lymphoid tissue. Measurements of plasma and urinary cortisol levels are obtained. Several blood samples may be collected to determine whether the normal diurnal variation in plasma levels is present; this variation is frequently absent in adrenal dysfunction. If several blood samples are required, they must be collected at the times specified, and the time of collection must be noted on the requisition slip

ITP nursing care/Pharmacological and Parenteral Therapies Contraindications

Monitor all secretions/body surfaces for bleeding Assess level of consciousness/VS q 4hr Limit invasive procedure - injections, surgery, enemas, suppositories, etc. Provide soft diets Use stool softeners Avoid valsalva maneuver - prevent straining, vomiting, sneezing, coughing, etc. Use of electric razors, soft toothbrushes/toothettes only Protect from falls/injury The nurse must be alert for sulfa-containing medications and others that alter platelet function (e.g., aspirin-based or other NSAIDs). Nursing Management Nursing care includes an assessment of the patient's lifestyle to determine the risk of bleeding from activity. A careful medication history is also obtained, including use of over-the-counter (OTC) medications, herbs, and nutritional supplements. The nurse must be alert for sulfa-containing medications and others that alter platelet function (e.g., aspirin-based or other NSAIDs). The nurse assesses for any history of recent viral illness and reports of headache or visual disturbances, which could be initial symptoms of intracranial bleeding. Patients who are admitted to the hospital with wet purpura and low platelet counts should have a neurologic assessment incorporated into their routine vital sign measurements. All injections or rectal medications should be avoided, and rectal temperature measurements should not be performed, because they can stimulate bleeding. Studies of patients with ITP have demonstrated a significant increase in fatigue compared to those without the disease that was not associated with the duration of the disease, corticosteroid use, bleeding episodes, and low platelet count (Diz-Küçükkaya & López, 2016). Nurses should explore the extent the patient experiences fatigue and offer strategies to ameliorate this problem. Patient education addresses signs of exacerbation of disease (e.g., petechiae, ecchymoses), how to contact appropriate health care personnel, the name and type of medication inducing ITP (if appropriate), current medical treatment (medications, side effects, tapering schedule if relevant), and the frequency of monitoring the platelet count. ****The patient is instructed to avoid all agents that interfere with platelet function, including herbal therapies and OTC medications. *****The patient should avoid constipation, the Valsalva maneuver (e.g., straining at stool), and vigorous flossing of the teeth. Electric razors should be used for shaving, and soft-bristled toothbrushes should replace stiff-bristled ones. The patient may also be counseled to refrain from vigorous sexual intercourse when the platelet count is less than 10,000/mm3. Patients who are receiving corticosteroids long term are at risk for complications including osteoporosis, proximal muscle wasting, cataract formation, and dental caries (see Table 52-5). Bone mineral density should be monitored, and these patients may benefit from calcium and vitamin D supplementation and bisphosphonate therapy to prevent significant bone disease.

failure to thrive interventions

NURSING INTERVENTIONS DURING THE CHILD'S HOSPITALIZATION FOR FAILURE TO THRIVE Observe parent-child interactions, especially during feedings. Develop an appropriate feeding schedule. Provide feedings as prescribed (usually 120 kcal/kg/day is needed to demonstrate proper weight gain). Weigh the child daily and maintain strict records of intake and output. Educate parents about proper feeding techniques and volumes. Provide extensive support to alleviate parental anxiety related to the child's inability to gain weight.

TOF Lab diagnosis

Note increased hematocrit, hemoglobin, and RBC count associated with polycythemia. Additional testing may include: Echocardiography (ultrasound study of structure and motion of heart), possibly revealing right ventricular hypertrophy, decreased pulmonary blood flow, and reduced size of the pulmonary artery Electrocardiogram (ECG), indicating right ventricular hypertrophy Cardiac catheterization and angiography, which reveal the extent of the structural defect The nurse is caring for a newborn with a heart defect that involves mixing blood from the pulmonary and systemic circulation. Which is a congenital heart disorder with mixed blood flow? Tetralogy of Fallo

Cushing's disease nursing management

Nursing Interventions DECREASING RISK OF INJURY Establishing a protective environment helps prevent falls, fractures, and other injuries to bones and soft tissues. The patient who is very weak may require assistance from the nurse in ambulating to avoid falling or bumping into sharp corners of furniture. Foods high in protein, calcium, and vitamin D are recommended to minimize muscle wasting and osteoporosis. Referral to a dietitian may assist the patient in selecting appropriate foods that are also low in sodium and calories. DECREASING RISK OF INFECTION The patient should avoid unnecessary exposure to others with infections. The nurse frequently assesses the patient for subtle signs of infection, because the anti-inflammatory effects of corticosteroids may mask the common signs of inflammation and infection. PREPARING THE PATIENT FOR SURGERY The patient is prepared for adrenalectomy, if indicated, and the postoperative course (see later discussion). If Cushing syndrome is a result of a pituitary tumor, a transsphenoidal hypophysectomy may be performed (see Chapter 66). Diabetes and peptic ulcer are common in patients with Cushing syndrome. Therefore, insulin therapy and medication to prevent or treat peptic ulcer are initiated if needed. Before, during, and after surgery, blood glucose monitoring and assessment of stools for blood are carried out to monitor for these complications. If the patient has other symptoms of Cushing syndrome, these are considered in the preoperative preparation. For example, if the patient has experienced weight gain, special instruction is given about postoperative breathing exercises. ENCOURAGING REST AND ACTIVITY Although the patient with Cushing syndrome experiences insomnia, weakness, fatigue, and muscle wasting, the nurse should encourage moderate activity to prevent complications of immobility and promote increased self-esteem. It is important to help the patient plan and space rest periods throughout the day and promote a relaxing, quiet environment for rest and sleep. PROMOTING SKIN INTEGRITY Meticulous skin care is necessary to avoid traumatizing the patient's fragile skin. The use of adhesive tape is avoided, because it can irritate the skin and tear the fragile tissue when the tape is removed. The nurse frequently assesses the skin and bony prominences and encourages and assists the patient to change positions frequently to prevent skin breakdown. IMPROVING BODY IMAGE If treated successfully, the major physical changes associated with Cushing syndrome disappear in time. The patient may benefit from discussion of the effect the changes have had on their self-concept and relationships with others. Weight gain and edema may be modified by a low-carbohydrate, low-sodium diet, and a high-protein intake may reduce some of the other bothersome symptoms. IMPROVING COPING Explanations to the patient and family members about the cause of emotional instability are important in helping them cope with the mood swings, irritability, and depression that may occur. Psychotic behavior may occur in a few patients and should be reported. The nurse encourages the patient and family members to verbalize their feelings and concerns. MONITORING AND MANAGING POTENTIAL COMPLICATIONS Addisonian Crisis. The patient with Cushing syndrome whose symptoms are treated by withdrawal of corticosteroids, by adrenalectomy, or by removal of a pituitary tumor is at risk for adrenal hypofunction and addisonian crisis. If high levels of circulating adrenal hormones have suppressed the function of the adrenal cortex, atrophy of the adrenal cortex is likely. If the circulating hormone level is decreased rapidly because of surgery or abrupt cessation of corticosteroid agents, manifestations of adrenal hypofunction and addisonian crisis may develop. Therefore, the patient with Cushing syndrome should be assessed for signs and symptoms of addisonian crisis as discussed previously. If addisonian crisis occurs, the patient is treated for circulatory collapse and shock (see Chapter 14). Adverse Effects of Adrenocortical Activity. The nurse assesses fluid and electrolyte status by monitoring laboratory values and daily weights. Because of the increased risk of glucose intolerance and hyperglycemia, blood glucose monitoring is initiated. The nurse reports elevated blood glucose levels to the primary provider so that treatment can be prescribed if indicated. PROMOTING HOME, COMMUNITY-BASED, AND TRANSITIONAL CARE Educating Patients About Self-Care. The patient, family, and caregivers should be educated that acute adrenal insufficiency and underlying symptoms will recur if medication is stopped abruptly without medical supervision. The nurse stresses the need for dietary modifications to ensure adequate calcium intake without increasing the risks for hypertension, hyperglycemia, and weight gain. The nurse educates the patient and family about how to monitor blood pressure, blood glucose levels, and weight. Patients should be advised to wear a medical alert bracelet and to notify other health care providers (e.g., dentist) about their condition (see Chart 52-12). Continuing and Transitional Care. The need for follow-up depends on the origin and duration of the disease and its management. The patient who has been treated by adrenalectomy or removal of a pituitary tumor requires close monitoring to ensure that adrenal function has returned to normal and adequacy of circulating adrenal hormones. Home care referral may be indicated to ensure a safe environment that minimizes stress and risk of falls and other side effects. The home care nurse assesses the patient's physical and psychological status and reports changes to the primary provider. The nurse also assesses the patient's understanding of the medication regimen and their compliance with the regimen and reinforces previous education about the medications and the importance of taking them as prescribed. The nurse emphasizes the importance of regular medical follow-up, the side effects and toxic effects of medications, and the need to wear medical identification with Addison and Cushing diseases. In addition, the nurse reminds the patient and family about the importance of health promotion activities and recommended health screening, including bone mineral density testing.

Liver failure/ ascites/ nursing care

Nursing Management If a patient with ascites from liver dysfunction is hospitalized, nursing measures include assessment and documentation of intake and output (I&O), abdominal girth, and daily weight to assess fluid status. The nurse also closely monitors the respiratory status because large volumes of ascites can compress the thoracic cavity and inhibit adequate lung expansion. The nurse monitors serum ammonia, creatinine, and electrolyte levels to assess electrolyte balance, response to therapy, and indications of hepatic encephalopathy

Liver failure/ esophageal Varices/ nursing care

Nursing Management Nursing assessment includes monitoring the patient's physical condition and evaluating emotional responses and cognitive status. The nurse monitors and records vital signs and assesses the patient's nutritional and neurologic status. This assessment assists in identifying hepatic encephalopathy. If complete rest of the esophagus is indicated because of bleeding, parenteral nutrition is initiated. Gastric suction usually is initiated to keep the stomach as empty as possible and to prevent straining and vomiting. The patient often complains of severe thirst, which may be relieved by frequent oral hygiene and moist sponges to the lips. The nurse closely monitors the blood pressure. Vitamin K therapy and multiple blood transfusions often are indicated because of blood loss. A quiet environment and calm reassurance may help to relieve the patient's anxiety and reduce agitation. Bleeding anywhere in the body is anxiety provoking, resulting in a crisis for the patient and family. If the patient has been a heavy user of alcohol, delirium secondary to alcohol withdrawal can complicate the situation. The nurse provides support and explanations about medical and nursing interventions to prepare both the patient and the family, because these procedures can be difficult to undergo and observe. Close monitoring of the patient helps in detecting and managing complications.

ITP nursing care /Potential for Complications of Diagnostics Tests/Treatments/Procedures

Nursing Management Nursing care includes an assessment of the patient's lifestyle to determine the risk of bleeding from activity. A careful medication history is also obtained, including use of over-the-counter (OTC) medications, herbs, and nutritional supplements. The nurse must be alert for sulfa-containing medications and others that alter platelet function (e.g., aspirin-based or other NSAIDs). The nurse assesses for any history of recent viral illness and reports of headache or visual disturbances, which could be initial symptoms of intracranial bleeding. Patients who are admitted to the hospital with wet purpura and low platelet counts should have a neurologic assessment incorporated into their routine vital sign measurements. All injections or rectal medications should be avoided, and rectal temperature measurements should not be performed, because they can stimulate bleeding. Studies of patients with ITP have demonstrated a significant increase in fatigue compared to those without the disease that was not associated with the duration of the disease, corticosteroid use, bleeding episodes, and low platelet count (Diz-Küçükkaya & López, 2016). Nurses should explore the extent the patient experiences fatigue and offer strategies to ameliorate this problem. Patient education addresses signs of exacerbation of disease (e.g., petechiae, ecchymoses), how to contact appropriate health care personnel, the name and type of medication inducing ITP (if appropriate), current medical treatment (medications, side effects, tapering schedule if relevant), and the frequency of monitoring the platelet count. The patient is instructed to avoid all agents that interfere with platelet function, including herbal therapies and OTC medications. The patient should avoid constipation, the Valsalva maneuver (e.g., straining at stool), and vigorous flossing of the teeth. Electric razors should be used for shaving, and soft-bristled toothbrushes should replace stiff-bristled ones. The patient may also be counseled to refrain from vigorous sexual intercourse when the platelet count is less than 10,000/mm3. Patients who are receiving corticosteroids long term are at risk for complications including osteoporosis, proximal muscle wasting, cataract formation, and dental caries (see Table 52-5). Bone mineral density should be monitored, and these patients may benefit from calcium and vitamin D supplementation and bisphosphonate therapy to prevent significant bone disease.

Abdominal aneurysm endovascular and surgical nursing care management

Perfusion Abdominal Aneurysm Endovascular and Surgical Management Nursing Care Before endovascular repair or surgery, nursing assessment is guided by anticipating a rupture and by recognizing that the patient may have cardiovascular, cerebral, pulmonary, and renal impairment from atherosclerosis. The functional capacity of all organ systems should be assessed. Medical therapies designed to stabilize physiologic function should be promptly implemented. Hemorrhage that leads to shock is a serious adverse consequence that must be treated decisively (see Chapter 14). The patient who has had an endovascular repair must lie supine for 6 hours; the head of the bed may be elevated up to 45 degrees after 2 hours. The patient needs to use a bedpan or urinal while on bed rest. Vital signs and Doppler assessment of peripheral pulses are performed initially every 15 minutes and then at progressively longer intervals if the patient's status remains stable. The access site (usually the femoral artery) is assessed when vital signs and pulses are monitored. The nurse assesses for bleeding, pulsation, swelling, pain, and hematoma formation. Skin changes of the lower extremity, lumbar area, or buttocks that might indicate signs of embolization, such as extremely tender, irregularly shaped, cyanotic areas, as well as any changes in vital signs, pulse quality, bleeding, swelling, pain, or hematoma, are immediately reported to the primary provider. The patient's temperature should be monitored every 4 hours, and any signs of postimplantation syndrome should be reported. Postimplantation syndrome typically begins within 24 hours of stent graft placement and consists of a spontaneously occurring fever, leukocytosis, and occasionally, transient thrombocytopenia. This condition has been attributed to complex immunologic changes that occur because of manipulations with sheaths and catheters with the aortic lumen, although the exact etiology is unknown. The symptoms are thought to be related to the activation of cytokines (Arnaoutoglou, Kouvelos, Koutsoumpelis, et al., 2015). They can be managed with a mild analgesic (e.g., acetaminophen [Tylenol]) or an anti-inflammatory agent (e.g., ibuprofen [Motrin]) and usually subside within a week. Because of the increased risk of hemorrhage, the primary provider is also notified of persistent coughing, sneezing, vomiting, or systolic blood pressure greater than 180 mm Hg. Most patients can resume their preprocedure diet and are encouraged to drink fluids. An IV infusion may be continued until the patient can drink normally. Fluids are important to maintain blood flow through the arterial repair site and to assist the kidneys with excreting IV contrast agents and other medications used during the procedure. Six hours after the procedure, the patient may be able to roll from side to side and may be able to ambulate with assistance to the bathroom. Once the patient can take adequate fluids orally, the IV infusion may be discontinued. Postoperative care requires frequent monitoring of pulmonary, cardiovascular, renal, and neurologic status. Possible complications of surgery include arterial occlusion, hemorrhage, infection, ischemic bowel, kidney injury, and impotence

Thoracic Aortic Aneurysm (TAA) manifestations

Symptoms vary and depend on how rapidly the aneurysm dilates and how the pulsating mass affects surrounding intrathoracic structures Some patients are asymptomatic In most cases, pain is the most prominent symptom. The pain is usually constant and boring but may occur only when the person is supine. Other conspicuous symptoms are dyspnea, the result of pressure of the aneurysm sac against the trachea, a main bronchus, or the lung itself; cough, frequently paroxysmal and with a brassy quality; hoarseness, stridor, or weakness or complete loss of the voice (aphonia), resulting from pressure against the laryngeal nerve; and dysphagia (difficulty in swallowing) due to impingement on the esophagus by the aneurysm

TOF pathophysiology

Tetralogy of Fallot is a congenital heart defect composed of four heart defects: 1. pulmonary stenosis (a narrowing of the pulmonary valve and outflow tract, creating an obstruction of blood flow from the right ventricle to the pulmonary artery) 2. VSD 3. overriding aorta (enlargement of the aortic valve to the extent that it appears to arise from the right and left ventricles rather than the anatomically correct left ventricle) 4.right ventricular hypertrophy (the muscle walls of the right ventricle increase in size due to continued overuse as the right ventricle attempts to overcome a high-pressure gradient). PATHOPHYSIOLOGY With pulmonary stenosis, the blood flow from the right ventricle is obstructed and slowed, resulting in a decrease in blood flow to the lungs for oxygenation and a decrease in the amount of oxygenated blood returning to the left atrium from the lungs. The obstructed flow also increases the pressure in the right ventricle. This blood, which is poorly oxygenated, is then shunted across the VSD into the left atrium. Poorly oxygenated blood also travels through the overriding aorta (if it extends to both ventricles). In some cases when the VSD is large, the pressure in the right ventricle may be equal to that of the left ventricle. In this case, the path of blood shunting depends on which circulation is exerting the higher pressure, pulmonary or systemic. Regardless of which way shunting occurs, a mixing of oxygenated and poorly oxygenated blood occurs, with this blood ultimately being pumped into the systemic circulation. The oxygen saturation of the blood in the systemic circulation is reduced, leading to cyanosis. The degree of cyanosis depends on the extent of the pulmonary stenosis, the size of the VSD, and the vascular resistance of the pulmonary and systemic circulations.

Hepatic encephalopathy manifestations

The earliest symptoms of hepatic encephalopathy include mental status changes and motor disturbances. The patient appears confused and unkempt and has alterations in mood and sleep patterns. The patient tends to sleep during the day and has restlessness and insomnia at night. As hepatic encephalopathy progresses, the patient may become difficult to awaken and completely disoriented with respect to time and place. With further progression, the patient lapses into frank coma and may have seizures Asterixis, an involuntary flapping of the hands, may be seen in stage II encephalopathy (see Fig. 49-13). Simple tasks, such as handwriting, become difficult. A handwriting or drawing sample (e.g., star figure), taken daily, may provide graphic evidence of progression or reversal of hepatic encephalopathy. Inability to reproduce a simple figure in two Or three dimensions is referred to as constructional apraxia. In the early stages of hepatic encephalopathy, the deep tendon reflexes are hyperactive; with worsening of the encephalopathy, these reflexes disappear and the extremities may become flaccid. Occasionally, fetor hepaticus, a sweet, slightly fecal odor to the breath that is presumed to be of intestinal origin, may be noticed. The odor has also been described as similar to that of freshly mowed grass, acetone, or old wine. Fetor hepaticus is prevalent with extensive collateral portal circulation in chronic liver disease

Shock preventing complications

The most common and serious side effects of fluid replacement are cardiovascular overload, pulmonary edema, and ACS. The patient receiving fluid replacement must be monitored frequently for adequate urinary output, changes in mental status, skin perfusion, and changes in vital signs. Lung sounds are auscultated frequently to detect signs of fluid accumulation. Adventitious lung sounds, such as crackles, may indicate pulmonary edema and ALI. Quality and Safety Nursing Alert When administering large volumes of crystalloid solutions, the nurse must monitor the lungs for adventitious sounds, signs and symptoms of interstitial edema, and work of breathing (i.e., increasing effort required for the patient to breathe). Often, a central venous pressure (CVP) line is inserted (typically into the subclavian or jugular vein) and is advanced until the tip of the catheter rests near the junction of the SVC and the right atrium. The CVP is used to assess preload in the right side of the heart. The CVP value assists in monitoring the patient's response to fluid replacement, especially when it is used in conjunction with additional assessment parameters (e.g., urine output, heart rate, BP response to fluid challenge) (Dellinger et al., 2013; Levy, Rhodes, Phillips, et al., 2015; Yealy, Kellum, Juang, et al., 2014). A normal CVP ranges from 4 to 12 mm Hg or cm H2O. Several readings are obtained to determine a range, and fluid replacement is continued to achieve a CVP between 8 and 12 mm Hg (Dellinger, 2015; Dellinger et al., 2013). Interpreting blood volume on the basis of CVP readings alone has been recently challenged in the literature; therefore, CVP readings should be used in conjunction with other assessment variables to assess blood volume (Levy et al., 2015; Marik, Some CVP catheters allow the monitoring of intravascular measures and venous oxygen levels. Assessment of venous oxygenation (venous oxygen saturation ([Sv_O2], or Scv_O2 with a CVP line) may be helpful in evaluating the adequacy of intravascular volume (Dellinger et al., 2013; Rivers, McIntyre, Morro, et al., 2005). Hemodynamic monitoring with arterial lines may be implemented to allow close monitoring of the patient's BP and tissue perfusion. A pulmonary artery catheter may be inserted to assist with closer monitoring of a patient's cardiac status as well as response to therapy. Advances in noninvasive or minimally invasive technology (e.g., esophageal Doppler, arterial pulse contour analysis, cardiac output devices, intrathoracic impedance monitoring) provide additional hemodynamic monitoring options (Cestero & Dent, 2015). (For additional information about hemodynamic monitoring, see Chapter 25.) Placement of central lines for fluid administration and monitoring requires collaborative practice between the provider and the nurse to ensure that all measures to prevent central line-associated bloodstream infection (CLABSI) are implemented. Several interventions aimed at preventing CLABSI should be implemented collaboratively while the central line is being placed as well as during ongoing nursing management of the central line itself. Chart 14-2 describes the evidence-based ("bundled") interventions that have been found to reduce CLABSI.

HELLP: therapeutic management

The treatment for HELLP syndrome is based on the severity of the disease, the gestational age of the fetus, and the condition of the mother and fetus. The mainstay of treatment is lowering of high blood pressure with rapid-acting antihypertensive agents, prevention of convulsions or further seizures with magnesium sulfate, and use of steroids for fetal lung maturity if necessary, followed by the birth of the infant and placenta (Foley et al., 2014). The client should be admitted or transferred to a tertiary center with a neonatal intensive care unit. Additional treatment includes correction of the coagulopathies that accompany HELLP syndrome. After this syndrome is diagnosed and the woman's condition is stable, birth of the infant is indicated. Magnesium sulfate is used prophylactically to prevent seizures. Antihypertensives such as hydralazine or labetalol are given to control blood pressure. Blood component therapy - such as fresh-frozen plasma, packed red blood cells, or platelets - is transfused to address the microangiopathic hemolytic anemia. Birth may be delayed up to 96 hours so that betamethasone or dexamethasone can be given to stimulate lung maturation in the preterm fetus

HIT treatment

Treatment for HIT includes prompt cessation of heparin (including any heparin-coated catheters) and initiation of an alternative means of anticoagulation. If the heparin is stopped without providing additional anticoagulation, the patient is at increased risk for developing new thrombi.**** Argatroban is an inhibitor of thrombin and an FDA-approved anticoagulant for the treatment of HIT. Oral anticoagulation with warfarin is contraindicated because it initially promotes thrombosis in the microvasculature by depleting protein C, which can lead to ischemia and gangrenous limbs (Greinacher, 2015). Once the platelet count has recovered, transitioning to treatment with warfarin is possible. Individuals who develop thrombosis in the setting of HIT should receive anticoagulation for 3 to 6 months; the duration of anticoagulation in the absence of thrombosis is shorter (Lee & Arepally, 2013). Patients need to be aware of their risk for reactivation Of the disorder should they be exposed to any amount of heparin within 3 to 4 months after diagnosis. This time frame is thought to be sufficient to remove anti-heparin-platelet antibodies from the circulation by the RES.

HELLP clinical presentation

abdominal pain and tenderness in the midepigastrium, RUQ or below the sternum; can also have N/V, malaise; can have hypertension >140/90 or proteinuria i. Pain may be caused by stretching of Glisson's capsule due perioportal or subcapsular bleeding or hepatic rupture Nursing assessment of the woman with HELLP is similar to that for the woman with severe preeclampsia. Be alert for complaints of nausea (with or without vomiting), malaise, epigastric or right upper quadrant pain, and demonstrable edema. Perform systematic assessments frequently, as indicated by the woman's condition and response to therapy. A diagnosis of HELLP syndrome is made based on laboratory test results, including: Low hematocrit that is not explained by any blood loss Elevated LDH (liver impairment) Elevated AST (liver impairment) Elevated ALT (liver impairment) Elevated BUN Elevated bilirubin level Elevated uric acid and creatinine levels (renal involvement) Low platelet count (less than 100,000 cells/mm3)

DIC risk factors

abruptio placenta AFE missed abortion fetal death in utero Severe preeclampsia or eclampsia (GHTN) Septicemia cardiopulmonary arrest hemorrhage Sepsis Trauma Cancer Shock Toxins Allergic reaction Infection DIC may be triggered by sepsis, trauma, cancer, shock, abruptio placentae, toxins, allergic reactions, and other conditions; the vast majority (two thirds) of cases of DIC are initiated by an infection or a malignancy

patent ductus arteriosus pathophysiology

passageway between the aorta and the pulmonary artery remains open after birth. Failure of the ductus arteriosus to close leads to continued blood flow from the aorta to the pulmonary artery. Blood returning to the left atrium passes to the left ventricle, enters the aorta, and then travels to the pulmonary artery via the PDA instead of entering the systemic circulation. This altered blood flow pattern increases the workload of the left side of the heart. Pulmonary vascular congestion occurs, causing an increase in pressure. Right ventricular pressure increases in an attempt to overcome this increase in pulmonary pressure. Eventually, right ventricular hypertrophy occurs. Oxygen supplementation is not helpful