Block 10 Part 2

Infective endocarditis treatment

*-Antimicrobials are the main treatment with the drug of choice depending on the organism involved; a significantly high dose must be given to ensure its destruction* -Antimicrobials are usually given IV with the course of treatment lasting 4-6 (2-8 on ppt) weeks; for most bacterial cases, the ideal antibiotic is one of the penicillins or cephalosporins; combination antibiotic therapy -Anticoagulants do not prevent embolization; these drugs are avoided unless they are required to prevent thrombus formation on a prosthetic valve -If antibiotic therapy is ineffective, vegetations are too large, or client develops HF, surgical intervention may be needed; infected valve may be removed -Valvular regurgitation (murmur) is the most common indication that there is a problem

Unstable VTach

*-Patient is symptomatic; Big change in LOC; Deterioration in vitals; BP is dumping! There IS A PULSE, but we need to change the rhythm!* *-Immediate CARDIOVERSION; Amiodarone- we may give amniodarone first as we are getting ready to cardiovert- just depends on state of patient, but CARDIOVERT is probably the first answer*; lidocaine *May sedate patient prior to cardiovert if VS are within acceptable range, however, MUST cardovert first if client is symptomatic* -We really can't think of comfort; potentially life threatening dysrhythmia!; Look at question!

Pulseless VTach

*CODE- Treat as VFib!* -Loss of consciousness with no pulse; rhythm will be rapid VTach, but there will be no pulse because internally, the heart is so chaotic that there is no cardiac output *Immediate CPR; Immediate Dfib= LOOK AT THE QUESTION to determine which is first (probably Dfib!); Start IV and administer drugs= amiodarone, lidocaine, epinephrine*

Addison's disease

*Decreased production of steriods= glucocorticoid (cortisol) and mineralcorticoid (aldosterone) resulting in decreased gluconeogenesis, carbs and protein (from decreased cortisol) and hypovolemia, hyponatremia, and hyperkalemia* *Signs and symptoms include: weakness, joint pain, anorexia and weight loss, N/V, bowel changes, dehydration, salt hunger, hypotension, hyperpigmentation, elevated K and Ca, decreased Na and glucose* *Patient is at risk for hypoglycemia, hypotension, hyperkalemia, and dehydration* *In an Addisonian crisis, there is a rapid onset of acute adrenal insufficiency which is a life threatening event in which the need for cortisol and aldosterone is greater than the supply; it often occurs during a stressful event; unless intervention is quick, sodium levels fall and potassium levels rise rapidly; severe vomiting and diarrhea result in severe hypotension and dehydration occurs; treatment is fluid with insulin- make sure an IV is in place, hydrocortisone IV; glucose as needed; antipyretics, antiemetics, continous cardiac monitoring* -ACTH stimulation test is the most definitive test for adrenal insufficiency; in insufficiency, the cortisol response is absent or very decreased *Treatment includes: steroid replacement therapy=mineralcorticoid (flourinef) and glucocorticoid (prednisode)- wean by giving in divided doses and monitor for hyperglycemia; monitor fluid balance, I&O, daily weights, monitor for dysrhythmias caused by lowered K levels; monitor minerals and electrolytes (K, Ca, Na)*

Cardioversion

*Delivery of a SYNCHRONIZED direct countershock to the heart using a lower amount of electricity, usually 500-100 joules* *Indicated for atrial dysrhythmias (AFib, AFlutter) if client is SYMPTOMATIC* -Goal is to return heart to normal rhythm- does not stop the heart! -Shock is synchronized on the r wave *must activate the sync button on the dfib machine* -For safety before cardioversion, turn off oxygen and away from patient; shout "clear" before shock delivery -Nursing care: maintain a patent airway, administer O2, assess vitals and LOC, administer antidysrhythmics, monitor for dysrhythmias, assess for chest burns, provide emotional support, document results

Defibrillation

*Delivery of an UNSYNCHRONIZED direct countershock to the heart* *Uses a higher amount of electricity- usually 200-300 joules* *Goal is to STOP the heart and STOP the chaotic rhythm and allow the SA node to take over to re-establish a perfusing rhythm* -Continue effective CPR until a defibrillator is available -*Synch button ON for Cardioversion and OFF for Defibrillation* -Charge machine -*Verify that all caregivers are "clear" and "away from client" and equipment connected to client* -Nursing care is the same as with Cardioversion -Document procedure from beginning to end; always document end of procedure rhythm, LOC, VS, O2 sat, and any complications

MI Rapid Nursing Assessment

*Rapid assessment of the patient with chest pain or other presenting symptoms is crucial; it is important to differentiate among the types of chest pain to identify the source* -Question the patient to determine the characteristics of the discomfort; Patients may deny pain, however, and report that they feel "pressure" -Ask questions about discomfort in terms of "PQRST" (pain, quality, radiation, severity, time) and onset of pain/duration (onset helps us with types of treatment) -Assess family history and client history (previous MI, risk factors, etc.) *Differentiate between angina pain and MI pain (HUGE!); Angina pain: substernal chest discomfort radiating to the left arm OR precipitated by exertion or stress (or rest in variant angina) OR relieved by nitro and rest OR lasting less than 15 min; few, if any associated symptoms; MI pain: Pain or discomfort in substernal chest pain/pressure radiating to the left arm OR pain or discomfort in jaw, back, shoulder, abdomen, OR, occuring without cause usually in the morning OR relieved only by opioids OR lasting 30 min or more; Frequent associated symptoms include: N/V, diaphoresis, dyspnea, feelings of fear/anxiety, dyrhythmias, fatigue, palpitations, epigastric distress, anxiety, dizziness, disorientation/acute confusion, feeling "short of breath"* *Many women experience atypical angina which manifests as indegestion, pain between shoulders, aching jaw, or choking sensation that occurs with exertion- these typically manifest during a stressful event or ADLs; women may curtail activity as a result; symptoms in women usually include fatigue, sleep disturbance, and dyspnea; In the older adult, pain may be diminished or absent-major manifestation in adults 80 and older may be disorientation or acute confusion because of poor cardiac output* -Discomfort from an MI does not usually resolve with nitro and rest -Ask about associated symptoms such as nausea, vomiting, diaphoresis, dizziness, weakness, palpitations, and shortness of breath -*Assess blood pressure and heart rate; interpret the patient's cardiac rhythm and presence of dysrhythmias; Sinus tachycardia with premature ventricular contractions frequently occurs in the first few hours of MI* -Assess distal peripheral pulses and skin temp; skin should be warm with all pulses palpable; in the patient with MI, poor cardiac output may be manifested by cool, sweaty skin and diminished or absent pulses -Auscultate for an S3 gallop which may indicate heart failure- a serious and common complication of MI -Assess respiratory rate and breath sounds for signs of heart failure; increased RR is common d/t anxiety and pain, but crackles or wheezes may indicate left-sided heart failure -Assess for JVD and peripheral edema -The patient with MI may experience temp elevation for several days after infarction; temps as high as 102 (38.9) may occur indicating the inflammatory response to the myocardial necrosis -Denial is common in the patient; on average, the patient with an acute MI waits more than 2 hours before seeking medical attention and rationalizes symptoms due to indigestion or overexertion

Stable VTach

*Signs and symptoms may be non initially other than patient feels palpitations; patient may be asymptomatic because they are getting cardiac output- MONITOR VITALS and LOC- we want to look for S&S* -Administer Oxygen -Check K levels -Drugs: Antidysrhythmics: *Amiodarone* (more popular because it works on atrial and ventricular dysrhythmias), Lidocaine (not first choice, only works on ventricular dysrhythmias and can make patient toxic) -ACLS guidelines state that elective cardioversion is highly recommended for VTach -Down the road, the patient may be a candidate for an Automated Internal Cardioverter Defibrilator (implantable device that monitors heart and shocks patient if needed)

Asystole

*The patient is in full cardiac arrest* -Truly the only arhythmia -Complete absence of any ventricular rhythm; there are no electrical impulses in the ventricles and therefore no ventricular depolarization , no QRS complex, no contraction, no cardiac output, and no pulse, respirations, or BP -Usually required for "confirmation" of death -Check 6 H's and T's -Called "flatlined" *Must confirm in 2 leads!!! One lead could show asystole, on could not or Could be fine VFib- this is your first action if you are unsure* Treatment: *First action is high-quality CPR- must have 100 compressions/min, must have recoil, must have good positioning, must have depth of 1 1/2-2 inches*; Establish IV and administer epi, vasopressin, atropine?; check for DNR status; consider termination status after appropriate standards have been met; *NO DEFIBRILLATION- NOT A SHOCKABLE RHYTHM!*

Nursing care of MI patient

*The primary goal of care for the MI patient is increased myocardial perfusion as evidenced by adequate cardiac output, normal sinus rhythm, and vital signs within normal limits* -Assess chest pain, associated symptoms, vitals, peripheral pulses, heart sounds, breath sounds, assess for presence of jvd/ peripheral edema -Subjective data= pain (PQRST), associated symptoms, personal and family history, etc. -Objective data= HR, diaphoresis, vitals, RR, N/V, pallor -Labs= Troponin I, CK-MB, Myoglobulins -Stat EKG and then serial EKGs -IV access -MONA (a stands for aspirin or anticoagulant-we may use heparin; oxygen 2-4 L) -Promote energy conservation (increased O2 demand on the heart) -Usually liquid diet for the first 24 hours -Prepare for reperfusion therapy *-Vital signs at least Q15 min*

Portal hypertension

-A persistent increase in pressure within the portal vein greater than 5 mm Hg and a major complication of cirrhosis -Results from increased resistance to or obstruction of the flow of blood through the portal vein and its branches -The blood meets resistance to flow and seeks alternative venous channels around the high pressure area -Blood flow backs into the spleen, causing splenomegaly -Veins in the esophagus, stomach, intestines, abdomen, and rectum become dilated -Portal hypertension can result in ascites, esophageal varices, prominent abdominal veins, and hemorrhoids -Patients with portal hypertension may also have *portal hypertensive gastropathy* which can occur with or without esophageal varices- in this condition, slow gastric mucosal bleeding occurs which may result in chronic slow blood loss, occult-positive stools, and anemia

Side effects of chemotherapy

-A serious complication of IV chemo infusion is extravasation; the most important nursing intervention for extravasation is prevention, therefore, close monitoring of the access site during chemo administration is critical -Temporary and permanent physical damage can occur to normal tissues from oral or IV chemo because it is systemic and exerts its effects on all tissues -Known problems include hemorrhagic cystitis, cardiac muscle damage, and loss of bone density -Serious short term side effects include anemia, neutropenia, and thrombocytopenia -Chemo destroys circulating blood cells and suppresses bone marrow function; reduced neutrophil numbers greatly increase risk for infection (neutropenia) and sepsis- this critical problem is the major dose-limiting side effect of cancer chemo and can lead to death during treatment -Common distressing side effects include nausea and vomiting, alopecia, mucositis (open sores on mucous membranes), many skin changes, anxiety, sleep disturbances, altered bowel elimination, and changes in cognitive function; these side effects are referred to as cancer therapy symptom distress-The priority care issues during chemo are protecting the patient from life-threatening side effects and managing distressing symptoms that occur with therapy -The most common infections are fungal, bacterial and some residual viral breakthrough- most infections during neutropenia result from overgrowth of the patient's own normal flora -Infection risk can be managed with the use of biological response modifiers (BRMs) and growth factors to stimulate bone marrow production of immune system cells; although not appropriate for all types of cancer, this supportive treatment can reduce the risk for infection during chemotherapy -Actual infections are treated with antibiotics, antifungals and antivirals just like any other infection; get a culture and sensitivity before administering antibiotics -The priority care issues during chemo are protecting the patient from life-threatening side effects and managing distressing symptoms that occur with therapy

Cardiac dysrhythmias

-Abnormal rhythms of the heart's electrical system that affects its ability to *effectively pump oxygenated blood* throughout the body -The abnormalities are the results of disturbances in electrical impulse formation, conduction, or both -Dysrythmias are classified by the site of origin= SA node, AV node, or ventricle; the name tells us where the problem is -Some dysrhythmias are threatening, some are not -Nurses priority for care in clients with dysrhythmias is to assess for complications and monitor the client for response to treatment

Contraindications to Thrombolytic therapy

-Absolute and Relative contraindications -Absolute: any prior intracranial hemorrhage; known structural cerebral vascular lesion (ex. arteriovenous malformation= AVM); known malignant intracranial neoplasm; ischemic stroke within 3 months EXCEPT acute ischemic stroke within 3 hours; suspected aortic dissection; active bleeding or bleeding diathesis- tendency to bleed (excluding menses); significant closed head or facial trauma within 3 months -Relative: History of chronic, severe, poorly controlled hypertension; severe uncontrolled hypertension on presentation (systolic greater than 180 or diastolic greater than 110); history of prior ischemic stroke within 3 months, dementia, or known intracranial pathology not covered in contraindications; traumatic or prolonged (over 10 minutes) CPR or major surgery; recurrent (within 2-4 weeks) internal bleeding; noncompressible vascular punctures; previous exposure (more than 5 days) or prior allergic reaction to streptokinase/anistreplase; pregnancy; active peptic ulcer; current use of anticoagulants (higher the INR, the higher the risk for bleeding)

Myesthenia Gravis

-An acquired autoimmune disease characterized by fatigue and weakness; the patient's own antibodies attack acetylcholine receptors in the muscle resulting in reduced to no contractions -May take many forms-from mild disturbances of the ocular muscles to a *rapidly developing generalized weakness that may lead to death from respiratory failure* -It has remissions and exacerbations -The thymus gland is often abnormal (hyperplasia) -Signs and symptoms include: *progressive muscle weakness; ptosis; weak or incomplete eye closure; diplopia, respiratory compromise; ocular palsies d/t damage of cranial nerve III, loss of bowel and bladder control; fatigue; difficulty chewing/swallowing; muscle achiness; parasthesias, decreased sense of smell and taste* *Management includes mechanical ventilation, thmectomy, plasmapheresis, immunosuppressants (corticosteroids); gamma globulins; ChE inhibitors (first line management) controlling the symptoms, positioning, monitoring I&O, neuro, and resp status; plasmapheresis may be done before and after a thymectomy to reduce circulating antibodies* -A potential adverse effect of ChE inhibitors is cholinergic crisis= sudden increases in weakness and inability to clear secretions, swallow or breathe adequately indicate the crisis -Myasthenic crisis is an exacerbation of the myasthenic symptoms caused by not enough ChE drugs; treat with ChE drugs and provide respiratory care -Cholinergic crisis is an acute exacerbation of muscle weakness caused by too many ChE drugs; treat with atropine and stop all ChE meds *After a patient receives a thymectomy, pay special attention to pulmonary hygiene; suction as needed and observe for signs of pneumo/hemothorax: chest pain, sudden SOB, absent breath sounds, restlessness or change in vital signs*

Emergency care of the patient with chest pain

-Assess airway, breathing and circulation; Defibrilate as needed -*Provide continuous ECG monitoring* -Obtain the patient's description of pain or discomfort -Obtain vitals -Assess and provide vascular access -Consult chest pain protocol or notify physician/rapid response for specific intervention -Obtain 12-lead EKG within 10 minutes of reports of chest pain -Provide pain relief (morphine) and aspirin as needed -Administer O2 to maintain sat at or above 95% -Remain calm and stay with patient if possible -Assess vitals and intensity of pain 5 minutes after admin of meds -Remedicate with prescribed drugs if vitals remain stable and check the patient every 5 minutes -Notify physician if vitals deteriorate

AAA manifestations

-Assess patients with a known or suspected AAA for abdominal, flank, or back pain; pain is usually described as steady with a gnawing quality, unaffected by movement, and lasting for hours or days -A pulsation in the upper abdomen may be present; a detectable aneurysm is at least 5 cm in diameter; auscultate for a bruit over the mass, but *avoid palpating the mass because it may be tender and there is a risk for rupture* -If expansion and impending rupture of a AAA are suspected, assess for severe pain of sudden onset in the back or lower abdomen which may radiate to the groin, buttocks or legs -Patients with a rupturing AAA are critically ill and in hemorrhagic (hypovolemic shock) -Signs and symptoms include: hypotension, tachycardia, diaphoresis, decreased LOC, feeling of impending doom, oliguria, SOB, loss of pulses distal to the rupture, dysrhythmias; retroperitoneal hemorrhage is characterized by hematomas in the flanks; rupture into the abdominal cavity causes abdominal distention -Watch for widening pulse pressure (take BP on both arms for any client with chest pain) -If patient is hypertensive, get blood pressure under control with a vasodilator (Nitroprusside)

Pacemakers

-Can be temporary, epicardial, or permanent -Electrodes are attached to the myocardial muscle on one side and connect to the pulse generator on the other side -Can be dual chamber (pace ventricles, atria, or both) -Can be set at a fixed rate; usually 70 bpm -Synchronous (or Demand) only fires if pt. heart rate falls below a certain level (usually 70 bpm) -Indicated for bradycardia, second degree or complete heart block, sick sinus syndrome (heart gets older and SA node doesn't fire as much), sinus arrest, asystole, atrial or ventricular tachycardias -Always look for pacemaker upon assessment of pt. -Avoid defibrillation over pacer site -Educate pt to report any S&S of dizziness, syncope, bradycardia -Monitor for complications of invasive temp. pacing such as etopic complexes, loss of capture (pacer spikes but no QRS), undersensing or oversensing; stimulation of chest wall or diaphragm (could cause cardiac tamponade) -Pacer spike should be in front of every QRS, if not, we don't have a good capture

Hypertrophic Cardiomyopathy

-Cardinal features are asymmetric ventricular hypertrophy and disarray of the myocardial fibers; ventricular walls are hypertrophied leading to smaller ventricular chambers; Left ventricular hypertrophy leads to a stiff left ventricle, which results in *diastolic/ventricular filling abnormalities* -Some patients die without any symptoms, whereas others have dyspnea on exertion, syncope, dizziness, and palpatations -Other symptoms include: angina, mild cardiomegaly, S4 gallop, ventricular dysrhythmias, heart failure -Many athletes who die suddenly probably had hypertrophic cardiomyopathy -Treatment includes: symptomatic treatment; beta blockers, conversion of a fib, calcium channel blockers, antidysrhythmics, surgery (ventriculomyotomy) or muscle resection with mitral valve replacement to increase ventricular outflow; nitrates and other vasodilators (contraindicated with obstructive form of disease)

Ascites

-Collection of free fluid within the peritoneal cavity caused by increased hydrostatic pressure from portal hypertension -Fluid shifts from the vascular system into the abdomen (a form of third spacing) due to decreased plasma proteins in the blood combined with decreased albumin production; this fluid shift results in a patient having hypovolemia and edema at the same time -Massive ascities may cause renal vasoconstriction, triggering the renin-angiotensin system which results in sodium and water retention; increasing hydrostatic pressure and vascular volume leads to more ascities -Massive ascites can be detected as a distended abdomen with bulging flanks; the umbilicus may protrude and dialated abdominal veins may radiate from the umbilicus -Ascites can cause physical problems such as orthopnea and dyspnea; the patient may have problems maintaining an erect posture and problems with balance may effect walking; inguinal or umbilical hernias may develop -Measure the patient's abdominal girth to evaluate the progression of ascites *however, taking daily weights is always the most reliable indicator of fluid retention*

Portal-Systemic Encephalopathy (PSE)

-Complex cognitive syndrome that results from liver failure and cirrhosis -Exact cause is unknown but may be due to higher levels of serum ammonia buildup that affect the brain although some patients may exhibit symptoms without increased ammonia levels; other factors include cirrhosis with: high protein diet, infection, hypovolemia, hypokalemia, constipation, GI bleed, drugs (hypnotics, opioids, sedatives, analgesics, diuretics, illicit drugs) -May develop slowly in patients with chronic liver disease and go undetected until the late stages; symptoms develop quickly in acute liver dysfunction -Patients report sleep disturbance, mood disturbance, mental status changes, and speech problems in the early stages; Later neurological symptoms include ALOC, impaired thinking processes, and neuromuscular problems -May be reversible with early intervention -4 stages of development: Prodromal (subtle behavior changes); Impeding (continuing changes including confusion and disorientation); Stuporous (progressive deterioration with marked mental confusion and stuporous behavior- drowsy but arousable); Comatose (unresponsiveness, leading to seizures and death) -The patient's symptoms may gradually progress to coma or fluctuate among the four stages; continually assess the patient's neurological function- subtle changes in mental status and personality often progress to coma

Coronary arteries

-Coronary blood flow to the myocardium occurs primarily through diastole, when coronary vascular resistance is minimized; to maintain adequate blood flow through the coronary arteries, MAP must be at least 60; A MAP between 60-70 is necessary to maintain perfusion of major body organs -The left main artery divides into LAD and LCX; The LAD branch descends toward the anterior wall and apex of the left ventricle; *Obstructions are the most serious here because they supply the anterior wall of the heart and most of the left ventricle; these clients have the highest mortality rate due to LV failure and ventricular dysrythmias (Vfib, VTach, 3rd degree heart block); in addition, because nothing goes forward, it must go backward (pulmonary edema, heart failure, etc.)* -The LCX branch descends toward the lateral wall of the left ventricle and apex. *It supplies blood to the lateral wall of the left ventricle and portions of the posterior wall and can develop posterior or lateral wall MI with sinus dysrythmias* -The right coronary artery encircles the heart, and descends toward the apex of the right venticle; *The RCA supplies the RV and SA and AV nodes and can develop inferior wall MIs with severe damage to the right ventricle; dysrythmias include bradycardias and 2nd degree heart block*

AAA interventions

-Fluids (if the patient hasn't dissected); watch volume -Blood products -Surgery: resection, graft, stents -Draw labs -Monitor electroytes -Blood band if anticipating transfusion -Watch for DIC if multiple blood products are given *-For patients with a rupturing AAA, emergency surgery is performed* -The most common surgery for AAA has traditionally be resection or repair (aneurysmectomy), but mortality rate for elective resection is high and markedly increases for emergency surgery -In AAA resection, the physician excises the aneurysm from the abdominal aorta to prevent or repair the rupture -Patients selected for endovascular stent grafts are generally at high risk for major abdominal surgery; the endovascular repair of AAAs has decreased the length of hospital stay for patients requiring repair of abdominal aneurysms, however, the patient needs to be closely monitored for the development of complications including: MI, graft occlusion or rupture causing hemorrhage, hypovolemia or renal failure, respiratory distress, paralytic ileus

Torsades de Pointes

-Hypomagnesemia problem in which rhythm twists and flips on electrical axes; can also be caused by certain antidysrhythmics such as amiodarone -Similar to Vtach, but won't respond to antidysrhythmics *-Treatment is Mag Sulfate 2 grams*

Pericarditis

-Inflammation of the lining surrounding the heart (pericardium) -Acute pericarditis is most commonly associated with infective organisms; post MI syndrome; post pericardiotomy syndrome; acute exacerbations of systemic connective tissue disease -Chronic pericarditis occurs when chronic pericardial inflammation causes a fibrous thickening of the pericardium; caused by TB, radiation therapy, trauma, renal failure, or metastatic cancer; the pericardium becomes rigid, preventing adequate filling of the ventricles and eventually resulting in cardiac failure *-Chest pain is the most common symptom of pericarditis; it is classically grating and oppressive (sharp and stabbing) and aggravated by breathing (mainly on inspiration), coughing and swallowing; the pain is worse when pt is in the supine position and may be relieved by sitting up and leaning forward; ask specific questions to evaluate chest discomfort TO DIFFERENTIATE IT FROM PAIN ASSOCIATED WITH MI* *-The most common physical finding that almost always confirms the diagnosis is the auscultation of a pericardial friction rub; it is an extra heart sound with scratchy, high pitched sound that is produced when the inflamed, roughened pericardial layers create friction as they rub together; sounds like "squeaky shoes"*

Assessment and Manifestations of Hypovolemic Shock

-Information about a patient's urine output is especially important in assessment because urine output is reduced in the first stages of shock, even when fluid intake is normal -Assign an RN rather than assistive personnel to take vitals of a patient who is at risk for or is suspected of having hypovolemic shock -Most manifestations are caused by the changes resulting from compensatory efforts; Signs of shock are first evident as changes in cardiovascular function; as shock progresses, changes in renal, resp, integument, musculoskeletal, and CNS become evident -Cardio changes begin with decreased MAP, leading to compensatory responses, thus the earliest signs of hypovolemic shock are cardiovascular -Assess peripheral pulses for rate/quality; in initial stages of shock, the pulse increases to keep cardiac output and MAP at normal levels even though the stroke volume per beat is decreased; *increased HR is the earliest manifestation of shock*; as shock progresses, pulses may be absent -When assessing the BP of a pt, consider their normal baseline (ex. 90/50 may indicate severe shock in one person and may be normal blood pressure in another) -Because changes in systolic BP are not always present in the initial stages of shock, use changes in pulse rate and quality as the main indicators of shock presence or progression; pulse pressure (difference between systolic and diastolic BP) will become narrower -O2 sat between 90-95 occur with non-progressive stage of shock; values between 75-80 occur with progressive stage; *any value below 70 is considered a life threatening emergency and may signal the refractory stage of shock* -Resp rate increases in compensation; when lactic acidosis is present, the depth increases as well -Kidney changes occur to compensate by saving body water; assess urine for volume, color, specific gravity, and presence of blood or protein; *decreased urine output is a sensitive indicator or early shock; measure urine output at least every hour; in severe shock, urine output may be absent* -Of the four vital organs, only the kidney can tolerate hypoxia and anoxia for up to one hour without permanent damage- after an hour, patients are at risk for AKI and kidney failure -CNS changes first manifest as thirst which is caused in response to loss of blood volume -Assess pt.'s LOC; cerebral hypoxia may cause restlessness, agitation, anxiousness or feeling of impending doom; LOC progresses to confusion to lethargy to somnolence and loss of LOC -Deep tendon reflexes may be weak or absent; have patient squeeze hands for assessment -*Changes in mental status may be early signs of shock* -Although no single lab confirms or rules out shock, changes in labs may support the diagnosis; ABGs may become abnormal, pH decreased, PaO2 decreased, and PaCO2 increased, H&H decrease if shock is caused by hemorrhage; H&H elevate if caused by dehydration or fluid shift

Cholecystectomy

-Laparoscopic cholecystectomy (lap chole) is a minimally invasive surgery and currently the "gold standard"; it is performed far more often than the traditional approach -Advantages include: uncommon complication, low death rate, rare bile duct injury, quick patient recovery, low post-op pain -Commonly done as a same-day procedure in an ambulatory setting -Removing the gallbladder w/ laparoscopic technique reduces the risk for wound complications -After the lap chole, assess the patient's O2 sat frequently until the effects of the anesthesia have passed; offer food and water when fully awake and monitor for N/V; keep HOB elevated and assist pt to bathroom to void; early ambulation promotes absorption of the carbon dioxide (from inflation of abdominal wall during surgery); IV pain control is usually not needed -Traditional cholecystectomy has greatly declined over the last 20 years and patients who require it usually have severe biliary obstruction; Patient care is similar to the care for any patient who has had abdominal surgery; priority care for a patient who received a t-tube for bile drainage it to avoid raising the drainage system above the site of insertion to prevent backup of bile into the surgical area thus causing infection- the t-tube may remain in place for over a week -Advise patients to avoid excessive fatty foods and recommend a weight loss program if pt is obese; teach pt. to keep incision clean and report any changes that indicate infection; *remind pt to report repeat abdominal or epigastic pain with vomiting that may occur several weeks to months after surgery which indicates postcholecsytectomy syndrome (PCS)* -Management of PCS depends on the exact cause, but usually involves ERCP to find the problem and repair it

AAA Post-op care

-Limit elevation of the bed to 45 degrees or less to avoid flexion of the graft -During the immediate post-op period, the patient's BP is monitored with an arterial catheter; continuous cardiac monitoring is used to detect any dysrhythmias -Hemodynamic monitoring is used to detect low cardiac output or other findings consistent with MI; other signs of MI include: chest pain, SOB, diaphoresis, anxiety and restlessness -A major priority for nursing care after AAA is to assess for signs of graft occlusion or rupture; assess vitals and circulation every 15 minutes for the first hour, and then hourly with assessment of pulses distal to the graft site (posterior tibial and dorsalis pedis pulses) -Report signs of graft occlusion or rupture including: Changes in pulses; Cool to cold extremities below the graft; White or blue extremities or flanks; Severe pain; Abdominal distention; Decreased urine output -Hypovolemia and acute renal failure may occur because of blood loss during surgery or if rupture occured; Assess urine output hourly; If urine output is *less than 50 ml/hr, notify surgeon immediately- note that in this case, 50 ml is the lowest value, not 30 ml*; monitor creatinine and BUN daily -Assess respiratory rate and depth every hour and auscultate breath sounds when patient arrives on unit and then every 4 hours to monitor for respiratory complications -The patient may be intubated; turn and suction as needed -Administer opioids for pain as prescribed -Encourage early mobility to prevent atelectasis and DVT and use of pillow to splint with coughing -Paralytic ileus is expected for 2-3 days; patients usually have an NG tube set to low suction until they pass gas; listen for bowel sounds and gas every 8 hours and report to physician when heard; prolonged absence of gas and presence of abdominal distention may indicate paralytic ileus or bowel infarction

Sepsis predisposing conditions

-Malnutriton -Immunosuppression -Large, open wounds -Mucous membrane fissures in prolonged contact with bloody or drainage soaked packing -GI ischemia -Exposure to invasive procedures -Malignancy -Over 80 years -Infection with resistant organisms (MRSA, VRE) -Receiving chemo -Alcoholism -DM -CKD -Transplant patient -Hepatitis -HIV/AIDS

Cirrhosis clinical manifestations

-Many early manifestations are vague and nonspecific due to the slow progression of the disease; the development of late signs of advanced cirrhosis (end-stage liver failure) usually causes the patient to seek medical treatment -Early signs we may assess for: Fatigue, Significant change in weight, GI symptoms such as anorexia and vomiting, Abdominal pain and liver tenderness (both of which may be ignored by the patient) -Late signs we may assess for: jaundice, dry skin, rashes, petechiae, ecchymosis, palmar erythema, spider angiomas, ascites, peripheral edema, osteoporosis, and vitamin deficiencies (esp. A, D, E, and K) -Observe for frank blood in vomitus or stool or by positive fecal occult blood test (caused by gastritis, stomach ulceration, or oozing esophageal varices) -Monitor for asterixis= a coarse tremor characterized by rapid, nonrhythmic extensions in the wrists and fingers

Key features of Cancer development

-Neoplastic cells originate from normal body cells -Transformation of a normal cell into a cancer cell involves mutation of the genes (DNA) of a normal cell -Only one cell has to undergo malignant transformation for cancer to begin -Benign tumors grow by expansion, whereas malignant tumors grow by invasion -Most tumors arise from cells that are capable of cell division *-A key feature of cancer cells is the loss of apoptosis (the ability to die); these cells have an infinite life span* -Tumors that metastasize from the primary site into another organ are still designated as tumors of the originating tissue -Primary prevention of cancer involves avoiding exposure to known causes of cancer/ Secondary prevention involves screening for early detection -Tobacco use is a causative or permissive factor in 30% of all cancers

MI patho

-Obvious physical changes do not occur in the heart until 6 hours after the infarction, when the infarcted region appears blue and swollen *-This is why we need to perform interventions within the first 4-6 hours of symptom onset; We want to save the heart from damage; Time is muscle!* *-By 2-3 months, the necrotic area develops into a shrunken, thin, firm scar changing the entire size and shape of the ventricle (remodling) which may decrease left ventricular function resulting in heart failure, increased morbidity/mortality; because scar tissue does not contract or conduct electricity, this area is often the cause of chronic ventricular dysrythmias surrounding the infarcted zone*; Thus we must intervene quickly to prevent tissue death -Extent of the (zone of ) injury depends on whether the patient has developed collateral circulation from chronic conditions or risk factors (HTN, smoking, etc); anerobic metabolism; workload demands on the myocardium (this is why we put patients on bedrest for the first 24 hours- to reduce oxygen demand, thus workload on the heart) -Hypoxia from ischemia may lead to local vasodilation of blood vessels and acidosis; potassium, calcium, and magnesium imbalances as well as acidosis at the cellular level may lead to changes in normal conduction and contractile functions; catecholamines (epinephrine and norepinephrine) are released in response to hypoxia and pain and may increase the heart's rate, contractility, and afterload; these factors increase oxygen requirements in the tissue that is already oxygen deprived

Atrioventricular blocks

-Occur when supraventricular impulses are excessively delayed or totally blocked in the AV node or intraventricular conduction system -Heart blocks often require immediate intervention, depending on the type and severity *SA node continues to function normally- atrias depolarize and P waves occur regularly, BUT because of the conduction dysfunction, ventricular depolarizations and QRS complexes are either delayed or blocked* -First degree heart block: all sinus impulses eventually reach the ventricle; No treatment indicated, however, careful monitoring is indicated; *If the rhythm change is the FIRST TIME, it MUST be reported to the cardiologist/PCP (make sure you report along with patient's LOC and vitals= ALWAYS in cardio!) -Second degree heart block (type 1): some sinus impulses reach the ventricles but others do not because they are blocked; *Prolongation of the PRI until a QRS (ventricular depolarization) is dropped; Usually no signs and symptoms; Treatment includes oxygen, check ventricular rate, check apical pulse for a full minute; Atropine to speed up heart; consider pacing -Second degree heart block (type 2): some sinus impulses reach the ventricles, some do not; *Sudden drop of a QRS without warning*; S&S include: lightheadedness, dizziness, syncope; Treatment includes: *Pacing!- may start with an external pacer but definitive treatment is internal implanted pacemaker; Careful monitoring and observation of client as this block may progress to third degree heart block* -Third degree heart block: complete heart block; none of the sinus impulses reach the ventricles; the ventricles are therefore depolarized by a second, independent pacemaker; *because the impulse is blocked, an "accessory" pacemaker in the lower chambers (ventricles) will activate the ventricles- these are known as "escaped rhythms"*; Since the "accessory" pacemaker is activated separately of the SA node, *there are essentially 2 separate rhythms going on at the same time* AKA- the ventricle has the ability to contract on its own if the SA node fails to reach it- but it does so randomly!; Patient may be asymptomatic or have: fatigue, dizziness, chest pain...or may be severe progressing to syncope, confusion, severe chest pain, and sudden death; Treatment is permanent pacemaker *-Remember: Gun for the P waves when identifying heart blocks- 1st degree and second degree heart block type 2, the P waves are consistent, In second degree type 1 and 3rd degree heart block, the Ps vary*

PCTA

-Percutaneous transluminal coronary angioplasty with stent placement -Used to reopen coronary artery -Must consider which lesions are treatable, amount of myocardial risk, location of lesion, size of lesion -Often used in conjunction with thrombolytic therapy -Before the procedure, the patient receives an initial dose of antiplatelet drugs; if there are any concerns the patient may need CABG, it is held until post-procudre; the platelet inhibition increases risk of post-op bleeding and patients should wait 5-7 days after dosing before undergoing CABG -During the procedure, a balloon tipped catheter is positioned in the artery; the balloon is inflated which flattens the plaque against the artery wall; a stent is positioned in the now unoccluded artery to keep it open *-The HCP usually prescribes a long-term nitrate and dual antiplatelet therapy with aspirin and clipridogel (plavix) after a PTCA* -Pre-procedure care includes: consent, patient teaching, plavix administration (dose depends on if a client has received a thrombolytic) -Post procedure care includes: IV heparin loading dose followed by continuous infusion; IV nitroglycerin (tridil) or cardizem are administered to prevent coronary artery vasospasms; *assess vital signs; monitor for reaction to contrast medium; monitor for hypotension and hypokalemia, assess groin site for bleeding; assess for CHEST PAIN; assess for reperfusion dysrythmias; report any of these findings to HCP or rapid response immediately*

Cirrhosis Nursing Interventions

-Priority problems for patients with cirrhosis include: Excess fluid volume related to third spacing of abdominal and peripheral fluid; Potential for hemorrhage due to portal hypertension; Potential for hepatic encephalopathy (PSE) due to shunting of portal venous blood and/or increased serum ammonia levels -Supportive measures to control ascites include: nutrition therapy, drug therapy, paracentesis, and respiratory support -Nutrition therapy includes low sodium, low protein or high protein diet (depending on what stage of liver failure and ammonia levels- may need moderate protein diet to maintain healing); vitamin supplementation; high carb, moderate fat -Monitor for peritonitis (flu like symptoms; decreased UO; low BP; tachycardia; rigid abdomen) -Paracentesis may be needed to remove abdominal fluid -Diuretics= Lasix and Aldactone as combo therapy; check daily weights, daily abdominal girth, daily I&O; document peripheral edema and assess electrolyte levels -Failing liver has difficulty metabolizing drugs so they should be used sparingly (particularly opiods, sedatives, and barbituates) -Watch ammonia levels (byproduct of protein); Lactulose promotes ammonia excretion in the stool by binding ammonia in the gut and then it is pooped out; watch for hypokalemia and dehydration from excessive stools -Listen to lung sounds often (every 4-8 hours) to determine if ascites has created pulmonary complications; check for crackles (hepatopulmonary syndrome) -Assess for bleeding; before inserting an NG tube or EGD scope- think about espophageal varices!; beta-blockers (such as propranolol) are usually prescribed to prevent bleeding; infection is one of the most common indicators that patients will have an acute variceal bleed, therefore, patients with GI bleeding should receive antibiotics on admission; endoscopic therapies, rescue therapies, vasoactive drugs, blood replacement, and NG tube placement may all be used for bleeding episodes -For pruritis r/t jaundice, teach pt to use cool rather than warm water on the skin and not to use a lot of soap- teach UAP to soothe skin with lotion -If medical management fails to control ascites, the HCP may chose to divert the ascites into the venous system by creating a shunt (transjugular intrahepatic portal systemic shunt= TIPS) which is a non-surgical procedure used to control ascites and reduce variceal bleeding -Teach pt to avoid all OTCs (esp NSAIDS); do not drink alcohol; take lactulose, beta blockers, and diuretics as prescribed; maintain well balanced, low sodium and moderate protein diet; recognize s&s of hepatic encephalopathy

Supraventricular Tachycardia

-Rapid stimulation of atrial tissue at a rate of 100-280 bpm -P waves may not be visible because they are embedded in the preceding T-wave -SVT may occur in healthy people, especially women -In patients with a sustained rapid ventricular response, asses for palpitations, chest pain, weakness, fatigue, SOB, anxiety, hypotension and syncope -Cardiovascular deterioration may occur if the rate does not sustain adequate blood pressure; the heart does not have enough time in between contractions for ventricular filling, thus cardiac output is decreased; In that case, SVT can result in angina, heart failure, and cardiogenic shock -In nonsustained or slower ventricular response, the patient may be asymptomatic except for occasional palpitations -Treatment includes: Find and eliminate the cause; Oxygen; Vagal maneuvers (things that slow the heart down like bearing down, plugging nose, etc.); carotid massage *performed by physician only*; antidysrhythmics= *adenosine is drug of choice- given IV slam in intervals of 6 mg, 6mg, 12mg*; overdrive pacing; Cardioversion *if severely symptomatic* -Hallmark= Tachycardia above the ventricle; Super skinny QRS

Cholecsytitis Management

-Risk factors include: "The four F's"= Female, Forty, Fat, Fertile; rapid weight loss or prolonged fasting; increased cholesterol; birth control use; cholesterol lowering drugs; family history; prolonged TPN; Crohn's disease; gastric bypass; sickle cell; diabetes; pregnancy -Ask patient to detail the pain (usual pattern is episodic- "gallbladder attacks") and ask whether GI symptoms occur when fatty foods are eaten -The severe pain of bilary colic is produced by obstruction of the gallbladder or movement of one or more stones; bilary colic may be so severe at times that it occurs with tachycardia, pallor, diaphoresis, and extreme exhaustion- assess the patient for possible shock caused by bilary colic and notify HCP or rapid response if these manifestations occur- stay with patient and lower the HOB -Labs may reveal elevated WBC (inflammation or infection); Elevated ALP (remember the bone growth or bone disease indication for elevation); Elevated AST and LDH; Elevated bilirubin; if pancreas is involved, Amylase and Lipase may be elevated -Stones that are not calcified cannot be seen- calcified gallstones are easily viewed on abdominal x-ray; US of the upper right quadrant is the best diagnostic test for cholecystitis; ERCP; MRCP (similar to MRI) -Surgery is the treatment of choice; most patients do not respond to nonsurgical interventions -Withhold food and fluids if nausea and vomiting occur; IV therapy is used for hydration -Acute biliary pain requires opioid anelgesia, such as morphine or hydromorphone (dilaudid); we no longer use demerol; ketorlac may be used for mild to moderate pain -Antiemetics for nausea/vomiting and IV antibiotic therapy may also be given -Extracorporeal shock wave lithotripsy (ESWL) can be used to break up gallstones in patients who are not good surgical candidates or those with small stones; Percutaneous transhepatic biliary catheter may also be used to open the blocked duct to allow bile flow -Surgical removal includes either a laproscopic cholecystectomy or a traditional cholecystectomy (less common)

Pancreatic cancer treatment

-Standard chemotherapy or radiation are used to shrink tumors but chemo has limited success in increasing survival time -Biliary stents may be placed percutaneously for patients who have biliary obstruction and are high surgical risks; these stents keep the biliary system open -Complete surgical resection of the pancreatic tumor offers the patient the only effective treatment but it is only done on small tumors -For larger tumors, a radical pancreatectomy or the Whipple procedure (pancreaticoduodenectomy) can be performed -The Whipple procedure involves extensive surgical manipulation and is used most often to treat cancer of the head of the pancreas; the procedure entails removal of the proximal head of the pancreas, the duodenum, a portion of the jejunum, the stomach, and the gallbladder with anastomosis of the pancreatic duct, the common bile duct, and the stomach to the jejunum; the spleen may also be removed -Complications of these procedures include: hemorrhage at anastomosis sites; MI; heart failure; thrombophlebitis; atelectasis; pneumonia; pulmonary embolism; ARDS; pulmonary edema; paralytic ileus; gastric retention or ulceration; bowel obstruction from peritonitis; acute pancreatitis; hepatic failure; thrombosis to mesentary; infection; dehiscence; fistulas (pancreatic, gastril, biliary); unstable DM; renal failure -The long and extensive open Whipple procedure can take many hours to complete and puts the patient at risk for significant fluid/blood and electrolyte loss; meticulous monitoring of volume is essential (vitals, I&O, swan-ganz catheter, H&H, lytes) -Watch for hyper/hypoglcemia after procedure (result of stress from surgery); monitor glucose levels closely during the early post-op period -The development of a fistula is the most common and most serious postoperative complication- the draining from a fistula cause leakage of bile, pancreatic enzymes, or gastric secretions which in turn causes chemical peritonitis; peritonitis will cause rigid, boardlike abdomen and requires antibiotics -If you suspect any postoperative complications resulting from these surgical procedures, notify HCP immediately

Coronary Artery Bypass Graft

-Surgery that restores myocardial perfusion by the addition of grafts bypassing the obstructed coronary arteries -Most common form of cardiac surgery; most common procedure for the older adult -Occluded arteries are bypassed with the patient's own venous or arterial vessels (saphinous vein or mammary artery) or synthetic grafts -Heart is temporarily stopped during surgery and circulation is created using a heart-lung machine -Once the grafts are attached and secured, the heart is started providing blood and oxygen to the body; the sternum is returned to its original position and closed -Indicated when patients do not respond to medical management of CAD or when disease progression is evident -Pre op includes: consent, teaching, splinting, coughing, deep breathing, pain management, pre-op labs, x-ray, EKG, other diagnostics -Post op includes: Usually on vent 3-6 hours post op (early extubation); *bleeding after CABG surgery occurs to a limited extent in all patients; measure mediastinal and pleural chest tube drainage OFTEN (at least hourly); report drainage amounts over 150 ml per hour to the surgeon; patients with mammry artery grafts may have more drainage than those with saphenous vein grafts; in addition, sudden cessation of drainage could indicate blood clot resulting in cardiac tamponade; maintain patency of chest tubes by preventing a dependent loop from forming; auscultate heart sounds (which may be muffled or decreased with cardiac tamponade); closely assess for dysrhythmias such as brady and afib or heart block; hypoxemia and hypokalemia are frequent causes of ventricular dysrhythmias; monitor for, report and document other complications of CABG including: fluid and electrolyte imbalance, hypotension, hypothermia, bleeding, cardiac tamponade, decreased LOC, anginal pain; managing fluid and electrolyte balance is a high priority- monitor BP, urine output and lytes; Monitor CBC, Coags, and blood sugar (which may fluctuate due to stress of surgery); monitor for chest pain and incisional pain, monitor LOC (check neuro Q 30-60 minutes until pt awakens from anesthesia, then check Q 2-4 hours; assess for and report any signs of cardiac tamponade including: sudden cessation of drainage, JVD but clear lung sounds, pulsus paradoxus, equalizing of PAWP and right arterial pressure, cardiovascular collapse; check temp (hypothermia is a significant risk for patient after CABG surgery because it promotes vasoconstriction and hypertension); manage pain and differentiate between sternotomy pain and anginal pain which may indicate graft failure- typical sternotomy pain is localized, does not radiate, and becomes worse with coughing or deep breathing*

Heart transplant

-Surgical replacement of a heart using a donor heart -Treatment of choice for a patient with severe dilated cardiomyopathy and may be considered for patients with restrictive cardiomyopathy -The procedure may also be done in patients with end stage heart disease d/t coronary artery disease, valvular disease, or congenital heart disease *-Criteria for candidate selection includes: life expectancy less than 1 year, age less than 65, NYHA class 3 or 4 (mostly bedbound), normal or only slightly increased pulmonary vascular resistance, absence of active infection, stable psychosocial status, no evidence of current drug or alcohol abuse* -Pre-op: Donor heart with compatible blood type and heart of comparable body weight; transplant usually done within 6 hours of harvesting; consent, labs, teaching, etc. -Post op: Be especially observant to identify occult bleeding into the pericardium with potential for cardiac tamponade; client may need a permanent pacemaker that is rate responsive to client's activity level; careful monitoring and aseptic technique for infection prevention- *infection is a major cause of death in heart transplants (unlike renal- rejection) and usually develops in the immediate post-transplant period; they will be on immunosuppressants for life* *-Heart transplant rejection signs and symptoms (very specific to heart); a lot are r/t ADLs: SOB, fatigue, fluid gain, edema, abdominal bloating, new bradycardia, afib, aflutter, hypotension, decreased activity level, decreased ejection fraction (late sign)* -Patients must have an aggressive, extensive and collaborative home health plan (teaching is huge!)

Sepsis with SIRS criteria

-Temp of more than 100.4 (38) or less than 96.8 (36) -Heart rate of more than 90 BPM -RR of more than 20 breaths/min or PaCO2 less than 32 -Abnormal WBC (greater than 12 or less than 4) *-Sepsis is considered present if two or more SIRS criteria are present along with any known infection and one or more of these clinical manifestations:* -Hypotension -Urine Output less than expected for fluid intake -Positive fluid balance -Decreased cap refill -Hyperglycemia (greater than 120 in absence of diabetes) -Unexplained change in mental status -Rising creatinine level in a person with no known kidney problems (over 2.0 in men/ over 1.4 in women)

Atrial Dysrhythmias

-The SA node fails to generate an impulse, the atrial tissue or areas in the internodal pathways may inflate an impulse -These are called atrial dysrhythmias -Generally not considered life threatening or lethal, however careful and deliberate client assessment should be continuous -With *Atrial Flutter*, there is rapid atrial depolarization; the AV node blocks the number of impulses that can reach the ventricle -Caused by Rheumatic or ischemic heart disease, heart failure, AV valve disease -Signs and symptoms include: palpitations, SOB, anxiety, syncope -Treatment includes: oxygen, Amniodarone, Cardizem, *Cardioversion if the client is severely symptomatic* -Hallmark of disease: Saw tooth P waves

Pericarditis treatment

-The focus of management of pericarditis is to relieve pain and treat the cause before severe complications occur -The HCP usually prescribes NSAIDs for pain and those who do not have bacterial pericarditis may receive steroids therapy -Assist patient to position of comfort (usually upright and forward) -Bacterial pericarditis (acute) requires antibiotics (2-6 weeks) and pericardial drainage -Definitive treatment for chronic pericarditis is surgical exision of the the pericardium (pericardiectomy) -Treatment of the underlying cause is essential *-Monitor all patients for pericardial effusion (pericardium fills with fluid) which puts the patient at significant risk for cardiac tamponade* -Cardiac tamponade is a medical emergency; it results from rapid accumulation of fluid in the pericardium which causes a sudden decrease in cardiac output; Findings include JVD, paradoxical pulse, decreased heart rate, dyspnea, fatigue, muffled heart sounds, hypotension -The physician may elect to perform a periocardiocentesis to remove fluid and relieve the pressure on the heart -*After the periocardiocentesis, closely monitor the patient for the recurrence of tamponade; pericardiocentesis alone does not resolve acute tamponade; be prepared to provide adequate fluid volume to increase CO and prepare patient for emergency sternotomy if tamponade recurs* -Avoid aspirin or anticoagulants because they may increase the possibility of tamponade

Acute Pancreatitis Clinical Manifestations

-The most common cause of Acute Pancreatitis is biliary tract disease, with gallstones accounting for almost half of the cases of obstructive pancreatitis -May result from trauma during surgical manipulation such as cholecystectomy or an ERCP -Other causes include: external trauma (gunshots, stab wounds, etc); hyperlipidemia, hyperparathyroidism, hypercalcemia; renal disturbances; genetics; ulcers resulting in peritonitis; viral infections; alcoholism; drug toxicities (opiates, sulfas, thiazides, steroids, contraceptives) -Pancreatitc "attacks" are especially common during holidays and vacations when alcohol consumption may be high -Signs and symptoms include: abdominal pain in mid-epigastric area or left upper quadrant that often has a sudden onset and radiates to the back, flank, or shoulder and is continuous and worsened by lying in supine position; weight loss from nausea/vomiting; jaundice; gray-blue discoloration of abdomen, periumbilical area, and flanks (caused by pancreatic enzyme leakage to the cutaneous tissue from the peritoneal cavity); listen for bowel sounds to detect ileus; note any tenderness, rigidity, or guarding; monitor vitals and assess for respiratory abnormalities by ascultating breath sounds -Monitor for significant changes in vital signs that may indicate shock; hypotension and tachycardia may result from pancreatic hemorrhage, excessive fluid volume shifting, or toxic effects of abdominal sepsis from enzyme drainage; observe changes in LOC that may be r/t alcohol withdrawal, hypoxia, or impending sepsis w/shock -Labs reveal increased Amylase levels (not completely specific and will be done with other tests to confirm diagnosis); increased Lipase levels (more useful in diagnosis because they stay elevated longer); increased bilirubin, ALP and ALT; increased WBC, ESR, and glucose; increased BUN and triglycerides; thrombocytopenia; decreased albumin; presence of C-reactive protein -Diagnostic tests include CT scan and abdominal X-ray and US

Care of the neutropenic patient

-The priority nursing interventions for the patient with neutropenia are protecting him or her from infection within the health care system and teaching the patient and family how to reduce infection in the home; total patient assessment including skin, mouth, lungs and IV insertion site should be performed every 8 hours by an RN for hospitalized patients -Meticulous handwashing and use of aseptic technique with any invasive procedure is essential infection prevention -Teach UAP the importance of mouth care and washing of axillary and perianal regions at least every 12 hours -Consider any temp elevation in a patient with neutropenia a sign of infection and report to HCP immediately; initiate infection protocol -Ensure patient's room/bathroom are cleaned at least once a day -Do not use supplies from common areas in the patient's room -Limit the number of health care personnel in the patient's room -Monitor vitals and check IV site every 4 hours -Inspect the mouth and any mucous membranes (especially anal area) for presence of fissures every 8 hours -Change wound dressings and IV tubing daily -Limit visitors to healthy adults -Monitor WBC (esp. neutrophils) daily -Avoid indwelling urinary catheters -Keep fresh flowers, potted plants, raw fruit and veggies, under cooked meat, eggs, fish, pepper and paprika away from patient -Encourage activity at appropriate level for patient as well as cough and deep breathe exercises

Dilated Cardiomyopathy

-The structural abnormality most commonly seen out of the myopathies -DCM involves extensive damage to the myofibrils and interference with myocardial metabolism -*Ventricular wall thickness is normal, but both ventricles are dilated, so systolic function is impaired leading to ineffective pumping* -Signs and symptoms include decreased cardiac output resulting in fatigue, palpitations, dyspnea on exertion, and exercise intolerance ; left sided heart failure, dysrhythnmias or heart block; systemic or pulmonary emboli; S3 and S4 gallops; moderate to severe cardiomegaly -May be caused by alcohol abuse, chemotherapy, infection, inflammation, and poor nutrition -Treatment includes: systemic treatment of heart failure; vasodilators, control of dysrhythmias, diuretics, or heart transplant

MI labs

-Troponin T and I are not found in the bloodstream of healthy people, so any rise in values indicates cardiac necrosis or MI; *very cardiac specific and will stay elevated longer* -Creatinine kinase MB (CK-MB) is *most specific to cardiac muscle, however does not peak until 24 hours after symptoms* -Myoglobulins are proteins found in cardiac and skeletal muscle; it is the *earliest marker detected, however, not specific to only cardiac muscle, therefore we would need another cardiac marker to indicate MI*

Cholecystitis (Acute)

-Two types: Calculous (most common) and Acalculous -Calculous cholecystitis results in chemical irritation and inflammation result from gallstones that obstruct the cystic duct, gallbladder neck, or common bile duct -When the gallbladder is inflamed, trapped bile is reabsorbed and acts as a chemical irritant to the gallbladder wall (a toxic effect from the bile occurs) -Reabsorbed bile, in combination with impaired circulation, edema, and distention of the gallbladder, causes ischemia and infection; the result is tissue sloughing with necrosis and gangrene; the gallbladder wall may eventually perforate (rupture); if the perforation is small and localized, an abscess may form; if the perforation is large, peritonitis may result -Acalculous cholecystitis is inflammation occurring without gallstones and is typically associated with bilary stasis (reduced blood flow to/reduced emptying of the gallbladder); most commonly occurs in patients with sepsis, severe trauma or burns, long term TPN, MODS, major surgery, or hypovolemia -Patients may present with abdominal pain, chest pain in between shoulders, pain triggered by a high-fat or high-volume meal, anorexia/nausea/vomiting, indigestion, gas, fullness, rebound tenderness, fever, jaundice, clay colored stools

MI diagnostics

1)-12 lead EKG examines and provides a graphic representation of the heart from various perspectives; *identifying the lead in which EKG change is occurring identifies both the occurrence and location of the ischemia or MI*; a rhythm strip is not a diagnostic tool, it is an identification tool- the 12 lead is diagnostic -*An ischemic heart does not repolarize normally, therefore, there are changes in the ST-segment; in other words, the ST segment represents a relaxed, filling ventricle; when it is ischemic and NOT relaxed, we will see things like ST-elevation* -In an infarction, there are 3 possible changes to the ST segment: -ST elevation (STEMI) -T wave inversion -Non-ST elevation (NSTEMI)- common in women -Also may develop pathological Q wave - usually means necrosis, "old MI", and may last for years on a 12 lead EKG; pathological Q waves are identified when width is more than one small square and depth is more than two small squares 2)-Exercise tolerance test (stress test) determines workload of the heart; preferred method; usually done after the acute stages of angina or an MI; traditionally done on a treadmill after pt. complains of fatigue or inability to perform ADLs; can be affected by obesity or age- in this case, we would use pharmacologic stress test (induce vasodilation/tachycardia) -Testing should not be done as a routine screening in asymptomatic patients; exceptions include very high risk of CAD or high risk occupations (airline pilots) 3)-Echocardiogram is an ultrasound of the heart; used to diagnose valve disease, heart failure, and cardiac tamponade (#1 tool for cardiac tamponade) 4)-Hemodynamic monitoring (Swan-Ganz Catheter); inserted via the jugular or subclavian and sits in the heart; provides info about blood volume, perfusion, fluid status, and how well the heart is pumping 5)-Coronary angiogram (cardiac cath) is the most definitive but most invasive test in the diagnosis of heart disease and MI; determines extent and exact location of coronary artery obstruction

Hepatitis A

A hardy virus that survives on human hands -Resistant to detergents and acids but destroyed by bleach and extremely high temps -Usually has a mild course similar to that of a typical flu-like infection and often goes unrecognized -Spread most often by the fecal-oral route either from person to person contact or by consuming contaminated food/water (commonly from shellfish contamination) -Incubation period is usually 15-50 days -Not life threatening but its course may be more severe in people older than 40 or with pre-existing conditions such as liver disease or Hep C; In a small percentage of people, severe illness with extrahepatic manifestations may occur requiring a liver transplant or causing death -Incidence of Hep A is particularly high in developing countries in which sanitation is poor -Some adults have Hep A and don't know it; the course is similar to that of a GI illness, and the disease and recovery are usually uneventful -Has reduced in US since CDC handwashing recommendations

Acute Pancreatitis

A serious, and at times, life threatening inflammatory process of the pancreas -Caused by premature activation of excessive pancreatic enzymes that destroy pancreatic cells, resulting in autodigestion and fibrosis of the pancreas (pancreas eats itself) -Severity depends on the extent of inflammation and tissue damage; can range from mild involvement (AEB edema and inflammation) to necrotizing hemorrhagic pancreatitis (NHP) whihc is diffusely bleeding pancreatic tissue with fibrosis and tissue death -The early activation of enzymes within the pancreas rather than the small intestine results in the inflammatory process of pancreatitis -Four major pathophysiologic processes occur: lipolysis, proteolysis, necrosis of blood vessels, and inflammation -The patient with hemorrhagic pancreatitis is critically ill, and extensive pancreatic destruction and shock leads to death; the majority of deaths in patients with acute pancreatitis results from irreversible shock -Complications include: pancreatic infection (causes septic shock); NHP; AKF; paralytic ileus; hypovolemic shock; pleural effusion; ARDS; atelectasis; pneumonia; MODS; DIC; type 1 or 2 diabetes; jaundice; intermittent hyperglycemia

Infective Endocarditis

AKA Bacterial Endocarditis -A microbial infection (usually strept or staph) involving any portion of the endocardium *-The heart valves are usually affected- primarily mitral* -Greatest risk factor is previous heart damage-primarily left side of heart (mitral valve) -Occurs primarily in patients who abuse IV drugs, have had valve replacements, have experienced systemic infection, or have structural cardiac defects -Bacteria enter through oral lesions, catheter insertion, surgery, UTI or URI and settle on valves and form a vegetative lesion; they colonize and ultimately scar and deform the valves *Heart failure is the most common complication of infective endocarditis* *Arterial embolization is a major complication in up to half of patients with endocarditis- occurs when fragments of vegetation break loose and move through bloodstream* *Key features include: FEVER ASSOCIATED WITH CHILLS, NIGHT SWEATS, MALAISE AND FATIGUE; anorexia and weight loss, cardiac murmur, development of heart failure; evidence of systemic embolization such as petichiae); splinter hemorrhages (black longitudinal lines or small red streaks under nails); osler's nodes (palms of hands and soles of feet); janeways lesions (reddened maculae on hands and feet); roths spots (whitish spots on retina); splenomegaly

Coronary Angiogram

AKA Cardiac Cath -The most definitive but most invasive test in the diagnosis of heart disease and MI -Studies right and left coronary arteries; can also determine valvular dysfunction *-Determines extent and exact location of coronary artery obstruction*; the injected dye will not pass through the blockages- this helps determine percentage of block -Allows cardiologist and surgeon to identify clients who might benefit from percutaneous angioplasty (PTCA) and stent replacement or from coronary artery bypass grafting (CABG) -When we see ST elevation in a 12 lead, it tells us what artery and maybe what part of heart is involved, but we don't know exactly what part of artery is involved or what percentage, this is why we need cardiac cath to show us -Assess client's knowledge and understanding of procedure (informed consent); *assess allergies-specifically shellfish*; explain sensations the client may experience during the procedure-palpations, salty taste, hot flashes; risks must be obtained by the cardiologist; obtain any labs or other diagnostics prior to the procedure -Complications include: thrombophlebitis, PE, vagal response; MI, CVA, arterial bleed or thromboembolism, dysrythmias, cardiac tamponade, hypovolemia, pulmonary edema, hematoma or blood loss at insertion site, reaction to dye -Post procedure: assess insertion site for swelling and bleeding, assess pedal pulses, keep limb straight; may be on bedrest for 2-6 hours; keep patient supine (may be elevated 30 degrees depending on physician preference); assess for chest pain, N/V; force fluids for dye excretion; *take vitals Q15 for 1 hour then Q30 for 2 hours or until vitals are stable, then Q4 or according to hospital policy*

Abdominal Aortic Aneurysm

Abdominal aortic aneurysms account for most aneurysms, are commonly aysmptomatic, and frequently rupture -Aneurysms cause symptoms by exerting pressure on surrounding structures or by rupturing -Rupture is the most frequent complication and is life threatening because abrupt and massive hemorrhagic shock results -Marfan syndrome, an inherited connective tissue disorder caused by a dominant gene is a major cause -Other causes include athersclerosis, hypertension, hyperlipidemia, smoking, blunt trauma, chronic inflammation of the aorta

Hepatitis clinical manifestations

Abdominal pain Changes in skin or sclera Arthraligia (joint pain) or myalgia (muscle pain) Diarrhea/constipation Changes in color of urine or stool Fever Lethargy Malaise Nausea/vomiting Pruritis Teach patients to: maintain adequate personal hygiene and handwashing; drink purified water; avoid food washed or prepared with tap water or ice from underdeveloped countries; use adequate sanitation practices; do not share bed linens, towels, eating utencils, or drinking glasses; do not share needles, razors, nail clippers, toothbrushes; use a condom or abstain from sex; cover cuts or sores with bandages; if ever infected, do not donate blood, body organs or other tissue; avoid all meds unless prescribed by physician; avoid all alcohol; rest frequently and eat small, frequent, well balanced meals -Immunoglobulin may be given within 14 days after exposure -Receive the vaccine if travelling to areas where disease is common or if living in or working in enclosed spaces -Chronic Hep B or C can be treated with antivirals and immunomodulation drugs -All cases of Hepatitis must be reported to the local health department

Diabetic Ketoacidosis and HHS

Acute condition characterized by *severe hyperglycemia (greater than 300, less than 600)*, breakdown of body fat for energy, *accumulation of ketones* in the blood and urine, and metabolic acidosis -DKA occurs most commonly in patients with type 1 DM but can also occur with type 2 patients under stress *The most common precipitating factor for DKA is infection; death occurs in 10% of these patients, even with appropriate intervention* -Hyperglycemia leads to osmotic diuresis with dehydration and electrolyte loss *Classic signs and symptoms of DKA include: polyuria, polydipsia, polyphagia, weight loss, vomiting, abdominal pain, dehydration, weakness, altered mental status, shock and coma; mental status can vary from total alterness to profound coma* *As ketone levels rise, the buffering capacity of the body is exceeded; the pH level decreases, and acidois occurs; Kussmaul Respirations (deep and rapid respirations) cause respiratory alkalosis as a compensatory mechanism* *Treatment includes: assessment of airway, LOC, hydration status, electrolytes, and glucose level; Assess VS q 15 min until stable; treat dehydration with LR or 0.9% NS (depending on sodium level); IV NS with insulin- when glucose is about 25o, change to D5 w/ 1/2 NS to prevent hypoglycemia and cerebral edema due to rapid decrease in osmotic pressure---Only give regular insulin IV- no Lantus!* *Monitor for adverse effects of therapy: hypokalemia (common cause of death in the treatment of DKA- before giving IV potassium, make sure patient is producing at least 30 ml/hr); monitor blood glucose for hypoglycemia; closely assess fluid status; monitor for fluid overload* *Teach patient sick day rules- continue Insulin regimen even when sick; closely monitor glucose Q4 hours; monitor urine for ketones; drink fluids and call MD if any signs of DKA* *Severe hyperglycemia (blood sugar over 600) without the presence of ketones and without acidosis is HHS* *HHS has a slow onset; may take hours or days to develop* *Signs and symptoms include: hypotension, tachycardia; all signs and symptoms of hyperglycemia; profound dehydration, K loss d/t osmotic diuresis; monitor for mental status changes, neuro deficits, seizures, coma* *Treatment is same as DKA; monitor electrolytes, I&O, EKG*

Guillain Barre Syndrome

Acute inflammatory demyelinating polyneuropathy that affects the peripheral nervous system -Demyelination of the peripheral nerves result in progressive motor weakness and sensory abnormalities *-Ascending paralysis that typically begins in the legs and spreads to upper arms and upper body (Respiratory system)- the brain receives fewer sensory signals affecting the client's ability to feel textures, heat and pain* *-Paralysis can increase in intensity until the muscles cannot be used at all; as a result, some patients require mechanical ventilation* -Signs and symptoms include ascending muscle weakness (tingling of lower extremities, numbness-wont be able to walk); will progress to bladder and bowel dysfunction, then to respiratory compromise; *Monitor vitals and the patient closely for varying blood pressure, hyper or hypotension and watch for dysrhythmias;* *Monitor respiratory status and promote airway patency and gas exchange; in the initial stage, monitor the patient for signs of respiratory distress such as dyspnea, air hunger, adventitious breath sounds, decreased O2 sat, and cyanosis; keep equipment for intubation at the bedside and have a vent readily available in case of respiratory emergency* *Treatment is centered around symptoms and complications: hypertension, depression-prozac, anxiety, seizure-phenytoin*; plasmapheresis

ALS

Also known as Lou Gherig's disease -An adult onset upper and lower motor neuron disease; lateral sclerosis refers to demyelination followed by hardening of the spinal column from buildup of scar tissue (myelin sheath is responsible for sending impulses- if it is hardened, that process does not happen) -Characterized by progressive muscle weakness, muscle wasting, and spasticity that eventually leads to paralysis -Beginning in one area of the body, motor weakness and deterioration spread until the entire body is involved, including the inability to talk, swallow and breathe -Death typically occurs within 3 years of diagnosis due to respiratory failure -The sensory and autonomic nervous systems are not involved, unlike other neural degenerative diseases -Key features include: tongue atrophy, weakness of hands and arms; beginning muscle atrophy of the arms; fasciculations (twitching of the face); nasal quality of speech; dysarthria (slurred speech), dysphagia; fatigue while talking *-There is no cure for ALS; Management is support of patient and family; Riluzole (Rilutek) can be used to extend survival time, however, it is not a cure (take without food and watch for liver toxicity)* -*At some point the patient will require ventilatory and nutritional support; the patient will need to be on a vent/endotracheal intubation/tracheostomy once respiratory muscles begin to weaken; feeding will need to be done through PEG tube* *-Hyperventilate the patient for 3-5 minutes or 100% O2 sat before suctioning; also listen for breath sounds before and after suctioning- cessation of rhonchi is an indicator that suctioning was successful*

Hepatic Abscess

Although not common, they carry a high mortality rate -Occur when the liver is invaded by bacteria or protozoa which destroy liver tissue, producing a necrotic cavity filled with infective agents and necrotic tissue walls off the abscess from the healthy liver -In pyogenic liver abscess, symptoms come on suddenly; In amebic hepatic abscess, symptoms develop slowly -Patients are generally quite ill and on occasion, the abscess is not diagnosed until autopsy -Look for peritonitis symptoms -Common manifestations include: Right upper abdominal pain with a palpable and tender liver; anorexia and weight loss; Nausea/Vomiting; Fever/Chills; Weakness/Malaise; Shoulder Pain; Dyspnea; Pleural pain if diaphragm is involved -Abscesses are usually drained under CT or US guidance and specimens sent to lab for proper antibiotic selection

Care of the thrombocytopenic patient

Anemia and thrombocytopenia also result from bone marrow suppression r/t some chemo drugs -Anemia causes the patient to feel fatigued, and some tissues are hypoxic -Thrombocytopenia increases risk for excessive bleeding -Both anemia and thrombocytopenia may require transfusion therapy -Growth factors to stimulate marrow production such as Epogen and Procrit may be used -The priority for nursing care for the patient with thrombocytopenia is to provide a safe hospital environment -Handle the patient gently and teach UAP to use a lift sheet when moving the patient -Avoid IM injections and venipunctures; when they are necessary, use the smallest needle for the task and apply firm pressure for 10 minutes to the needle stick site -Apply ice to areas of trauma -Test all urine and stool for occult blood -Observe IV sites every 4 hours for bleeding -Avoid trauma to rectal tissues (no enemas/ lubricate suppositories well) -Measure abdominal girth daily -Instruct pt to use electric shaver and soft bristled toothbrush -Instruct pt not to blow nose or insert objects into the nose -Instruct pt to wear shoes when ambulating and to keep pathways clear and uncluttered

Esophageal varicies

As a result of portal hypertension, the blood backs up from the liver and enters the esophageal and gastric veins -Esophageal varices occur when fragile, thin walled esophageal veins become distended and tortuous from increased pressure -The potential for varices to bleed depends on their size; *bleeding esophageal varices is a life threatening medical emergency- severe blood loss may occur, resulting in shock from hypovolemia*; the bleeding may either be hematemesis (vomiting blood) or melena (black, tarry stools) -Variceal bleeding can occur spontaneously without any precipitating factors; loss of consciousness can occur before any observed bleeding; however, any activity that increases abdominal pressure may increase the likelihood of a variceal bleed such as: heavy lifting/exercise, chest trauma, dry, hard food in the esophagus or NG tube placement *Splenomegaly* can result from the backup of blood into the spleen; the enlarged spleen destroys platelets causing thrombocytopenia and increased risk for bleeding *-Thrombocytopenia is often the first clinical sign that a patient has liver dysfunction*

Post MI meds

Beta blockers= decrease size of infarct; decrease occurrence of ventricular dysrythmias; decrease heart rate and contractility *beta blockers are significant in reducing a second coronary artery event- we need to teach this to pt. so they understand how important it is to take them* ACE or ARB= prevent ventricular remodeling; decrease development of heart failure; Monitor BP and HR CCB= decrease contractillity and excitability; decrease coronary vasospasms; we use these a lot immediately after MI, but patients are usually sent home with beta blockers and ACE or ARB

Sympathetic tone

Blood vessels are innervated by the sympathetic division of the autonomic nervous system -Some nerves continuously stimulate vascular smooth muscle so that the blood vessels are normally partially constricted (sympathetic tone) -Increases in sympathetic stimulation constrict smooth muscle even more, raising MAP while decreases relax smooth muscle, dilating blood vessels and lowering MAP -Blood flow to organs varies and adjusts to changes in tissue oxygen needs; the body can selectively increase blood flow to some areas while reducing blood flow to others (shunting); the skin and skeletal muscles can tolerate low levels of oxygen for hours without dying or being damaged, while other organs (heart, brain, liver, pancreas) do not tolerate being hypoxic and only a few minutes without oxygen results in serious cell damage and cell death

SIADH in cancer

Cancer is a common cause of syndrome of inappropriate diuretic hormone which causes increased secretion of ADH; it is commonly seen in patients with small cell lung cancer or cancers in the brain -In SIADH, water is reabsorbed to excess by the kidney and put into systemic circulation; the retained water dilutes blood serum sodium levels -Mild manifestations include weakness, muscle cramps, loss of appetite and fatigue -Serum sodium levels range from 115-120 or lower; with greater fluid retention, weight gain, nervous system changes, personality changes, confusion and extreme muscle weakness -As the sodium level drops to 110, seizures, coma, and death may follow, depending on how rapidly the sodium value is lowered -SIADH is managed by treating the condition and the cause -Nursing priorities focus on patient safety, restoring normal fluid balance, and providing supportive care -Management includes fluid restriction, increased sodium intake, and drug therapy -Demeclocycline (Declomycin) works in opposition to ADH -Patient safety includes preventing fluid overload from becoming worse, leading to pulmonary edema and heart failure; those with preexisting conditions as well as the older adult are at risk for greater complications -Monitor for increasing fluid overload (bounding pulse, JVD, crackles, increasing peripheral edema, reduced urine output) at least every 2 hours -Pulmonary edema can occur very quickly and lead to death; notify the HCP of any change that indicates the fluid overload from SIADH is not responding to therapy or is becoming worse

Liver Cancer

Cancers may be primary tumors (originating in the liver) or metastatic (spread from another organ to the liver) -In the US and worldwide, liver cancer is increasing d/t increased rates of hepatitis C (Chronic infection w/ Hep B and/or C leads to cirrhosis which is a risk factor for liver cancer -In the early stages, most patients are asymptomatic; Later, they report weight loss, anorexia, and weakness -Elevated AFP (a tumor marker for cancers of the liver and some other organs) and increased ALP are common -Surgical resection and liver transplantation are the only treatment for long term survival; unfortunately, most patients are not candidates for surgical removal because their tumors are unresectable -Chemo can be administered but is not effective in many cases -Patients with advanced liver cancer usually need end of life care and hospice services

Key features of shock

Cardiovascular: decreased cardiac output; increased pulse rate; thready pulse; decreased blood pressure; narrowed pulse pressure; postural hypotension; low central venous pressure; flat neck and hand veins in dependent positions; slow cap refill in nail beds; diminished peripheral pulses Respiratory: increased respiratory rate; shallow breathing; increased PaCO2; decreased PaO2; cyanosis-especially around the nail beds and lips Neuro: (early) anxiety; restlessness, increased thirst; (late) decreased CNS activity- lethargy to coma; generalized muscle weakness; diminished or absent deep tendon reflexes; sluggish pupillary response to light Renal: decreased urine output; increased specific gravity; sugar and acetone present in urine Integumentary: cool to cold; pale to mottled to cyanotic; moist/clammy; dry mouth/ paste-like coating present GI: decreased motility; diminished or absent bowel sounds; nausea and vomiting; constipation

Brain injury

Caused by a blow or jolt to the head or by penetration of foreign object; as a result, the normal functioning of the brain is disrupted -Nursing priority is to prevent life threatening complications (IICP) *Rhinorrhea and ottorhea are clinical signs of CSF leakage in patients with skull fracture; Presence of glucose in CSF is a diagnostic feature; CSF leakage opens the brain and spinal cord canal to infection (meningitis); Normal CSF is less than 15; anything above 20 is indicative of IICP* *Halo sign (clear drainage that separates from bloody drainage suggests presence of CSF)* *IV steroids DO NOT help ICP in brain trauma (problem is fluid, not necessarily tissue- give steroids after mannitol); Mannitol (osmitrol) is the osmotic diuretic drug of choice- used to decrease cerebral edema-dissolve crystals by submerging container in warm water if needed; Opiates should be avoided; Dilantin IV- must be given slowly- risk for hypotension* *Airway management and stabilization are priority- assess for airway by asking patient to tell you their name; use a cervical collar to stabilize; keep BP down; monitor electrolytes (r/t taking osmotic diuretic); monitor catheter and maintain patency (risk of catecholamine release leading to HTN)* *Monitor vitals and glasgow coma q 15 min- changes in baseline must be reported; maintain immobilization; avoid sneezing or coughing; avoid meds that decrease LOC* -Brain herniation occurs when a part of the brain pushes downward inside the skull through the opening into the neck; the more severe the herniation, the more serious and life threatening; *apnea alternating with periods of rapid breathing (cheyne-stokes respirations) indicates brain stem damage and imminent death* *Early signs and symptoms of IICP include: Slight LOC changes (MOST IMPORTANT!); sluggish pupils; impaired eye movement; changes in posturing (decerebration=extension/more severe and serious/decortication=flexion); headache; Cushing's Triad= HTN, widened pulse, decreased HR, irregular resp rate/rhythm; increased temp= all due to decreased cerebral blood flow*

Fatty Liver (Steatosis)

Caused by the accumulation of fats in and around the hepatic cells -May be caused by alcohol abuse or other factors such as diabetes, obesity, elevated lipid profile -Many patients are asymptomatic; the most common finding is elevated ALT and AST or normal ALT and elevated AST -MRI, US, percutanous biopsy can be used to confirm excessive fat in the liver -Interventions are aimed at removing the underlying cause -Weight loss, glucose control, and aggressive treatment using lipid-lowering agents are recommended -Monitoring liver function tests is essential in disease management

Pheochromocytoma

Chatecholamine producing tumor that arises in the adrenal medulla -The tumors produce, store, and release epinephrine and norepinephrine; excessive epi and norepi stimulate adrenergic receptors and can have wide ranging adverse effects -If undiagnosed/untreated, can lead to severe cardiac and neuro damage *Signs and symptoms include: HTN, severe headache, palpitations, chest/abdominal pain with N/V, diaphoresis, flushing, apprehension (feeling of impeding doom), heat intolerance, weight loss, and tremors; SATA!!!* *The most common diagnostic test is a 24 hour urine collection to test for vanillylmandelic acid (VMA)- a breakdown of catecholamines- high levels of VMA indicate pheochromocytoma* *Surgery is the main treatment (unilateral or bilateral adrenalectomy; meds= phenoxybenzamine (Dibenzyline) to control BP starting several weeks before surgery* *Do not palpate the abdomen of a patient with a pheochromocytoma- this action could cause sudden release of chatecholamines and trigger severe hypertension*

Care of patient with CINV

Chemotherapy-induced nausea and vomiting (CINV) arises from a variety of GI and neural mechanisms -Most chemo drugs are emetogenic (vomit inducing) to some degree depending on the dose -Most drugs induce nausea and vomiting when the drug is given and for 1-2 days afterward; some drugs can delay N/V for 5-7 days after receiving it -One or more antiemetics are usually given before, during, and after chemotherapy; patient response is variable and drug combinations are individualized for the best effect -Regardless of which drugs are being used to prevent or reduce CINV, they are most effective when used aggressively and on a scheduled basis -Drug therapy for CINV works best when given before the N/V are out of control, thus the nursing priority is to coordinate with the patient and HCP to ensure adequate control of CINV; ensure that antiemetics are given before chemo; teach patients to continue the prescribed therapy, even when CINV appears controlled -When the patient stops taking the drug, teach him or her to start retaking it at the first sign of nausea to prevent it from getting out of control -CAM therapies such as music, guided imagery and drinking concord grape juice before meals may help reduce N/V -Drugs for CINV include: Serotonin Antagonists; Neurokinin Receptor Antagonists; Corticosteroids; Prokinetic Agents and Benzodiazepines

Care of patient with CIPN

Chemotherapy-induced peripheral neuropathy is the loss of sensory or motor function of peripheral nerves associated with exposure to certain anticancer drugs -Although most commonly seen in patients with diabetes, the nerve-damaging drugs for cancer often cause rapid and severe CIPN in the chemo patient; higher doses lead to greater neuropathy -The most common problems include loss of sensation in hands and feet, orthostatic hypotension, erectile dysfunction, neuropathic pain, loss of taste discrimination, and severe constipation -CIPN is a long term consequence and may be permanent in some people; no known interventions prevent CIPN -The priority for nursing care of patients with CIPN is teaching them to prevent injury -Teach patient to always wear appropriate sized shoes and not to walk around without shoes on -Avoid pointed toe or heeled shoes -Inspect feet daily for open areas or redness -Avoid extreme temps and wear warm clothing in the winter -Use potholders when cooking and gloves when washing dishes -Eat foods high in fiber and allow food to cool before eating -Drink 2-3 liters of fluid a day -Get up from lying position slowly -Avoid area rugs and use handrails when using stairs or steps

Multiple Sclerosis

Chronic autoimmune disease that affects the myelin sheath; it is characterized by an inflammatory response that results in diffuse, random or patchy areas of plaque in the CNS which damages the myelin sheath and reduces its thickness (demyelinization) -The areas particularly affected are the optic nerve, spinal cord, and brain stem *- MS is a descending disease that attacks the brain first and client demonstrates dysphagia/optic nerve disorders and respiratory problems BEFORE weakness of extremities (unlike Gullian Barre Syndrome), therefore, the majority of symptoms are due to the descending nature of the disease* *MS can progress steadily or cause acute attacks (exacerbation) followed by partial or complete reduction in symptoms (remission)* -Signs and symptoms include: *blurred vision (fall risk, have things closer to pt.); diplopia (eye patch/cover one eye); for peripheral visual defecits, teach patient scanning techniques by moving head side to side*; decreased visual and hearing acuity; nystagmus (involuntary rapid eye movement); scotomas (patches in visual field); dysarthria; dysphagia; dysmetria; tinnitus; ataxia; muscle weakness; parasthesias; fatigue; GI disturbance; sexual dysfunctions; cognitive changes *Treatment is supportive; often times exacerbations are due to stress; control and treat symptoms and prevent complications (safety, skin breakdown, infection, PEG for dysphagia, etc.); Meds for management include baclofen (antispasmodic), NSAIDS, analgesics, corticosteroids, antidpressants; k channel blockers (amiodarone); beta blockers, anticonvulsants, anticholinergics (pro-banthine to decrease oral secretions or bladder dysfunction)*

DIC

Disseminated Intravascular Coagulation -Formation of thousands of small clots in the tiny capillaries of the liver, kidney, brain, spleen, and heart -DIC reduces oxygenation and decreases oxygen saturation, causing hypoxia and ischemia -The huge number of clots use clotting factors and fibrinogen faster than they can be produced; this problem increases the risk for hemorrhage, which occurs in the septic shock stage (patient will bleed from everywhere- even with non-invasive procedures) -Coupled with continued capillary leak, the bleeding causes hypovolemia and a dramatic decrease in cardiac output, BP, and pulse pressure; manifestations of this stage are the same as those of the later stages of hypovolemic shock Causes include: infection, surgery, blood transfusions, cancer, childbirth, sepsis, lupus, liver failure Treatment includes: platelets, plasma, heparin (if identified in the clotting stage- this is still a controversial treatment)

Sepsis manifestations and assessment

Early detection of sepsis before progression to septic shock is a major nursing responsibility -Because sepsis can be a complication of many conditions in the acute care setting, always consider its possibility -Review labs (esp. lactate levels) and monitor vitals frequently *-The hallmark of sepsis is an increasing lactate level, a normal or low WBC, and a decreasing segmented neutrophil level with a rising band neutrophil level (LEFT SHIFT)* -Sepsis and septic shock differ from other types of shock in many ways; the entire syndrome may manifest over many hours to days and the manifestations are less obvious -Cardiovascular changes include lower cardiac output and BP in the early stages and high cardiac output with vasodilation in the later stages which makes the skin pink and warm to the touch- this is temporary however, and eventually, the cardiac output is greatly reduced; DIC occurs with progression reducing oxygenation and tissue perfusion -Respiratory changes are first caused by compensatory mechanisms trying to maintain oxygenation with a rate increase; lungs are susceptible to damage and ARDS may occur as a result of continued SIRS; ARDS in a patient with septic shock has a high mortality rate -Skin changes range from pallor, cyanosis, mottling, and eccymoses (from DIC) -Low urine output in a patient with no know kidney problems may indicate shock; kidney function can decrease and creatinine levels will increase

Initial stage of shock (early stage)

Early or Initial stage of shock is present when the patient's baseline MAP is decreased by less than 10 mm Hg -During this stage, compensatory mechanisms are so effective at returning systolic pressure to normal that oxygenated blood flow to vital organs is maintained (cardiac output and MAP remain within normal range) -Cellular change is increased anaerobic metabolism with production of lactic acid, although overall metabolism is still aerobic -Because vital organ function is not disrupted, the manifestations of shock are difficult to detect at this stage -A heart rate (higher than 90 bpm) or respiratory rate (higher than 20 breaths/min) increased from the patient's baseline level or a *slight increase* in diastolic blood pressure may be the only manifestation of this early stage of shock -We might see an elevation/or decrease in temp (above 38 or below 36 degrees Celsius); an increase in lactate or lactic acid (normal range is 0.3-2.6); an increase or decrease in WBC count -Assess for shock in any patient who develops a change in mental status, an increase in pain, or an increase in anxiety (facility screening tools can help with this) -If symptoms are recognized at this stage, apply oxygen, notify HCP and implement facility protocol for sepsis or shock; give antibiotics (big guns= vanco, tobramycin, zosin, etc.- know pt. drug allergies); give fluids (can give lasix later if we overload); find the problem and fix it!

Cushing's Disease

Exaggerated secretion of cortisol from the adrenal cortex, causing widespread problems -The presence of excess glucocorticoids, regardless of the cause, affects metabolism and all body systems; high levels of cortisol reduce both inflammatory and immune response *Signs and symptoms include: fat redistribution (moon face, buffalo hump, truncal obesity); thinner lower extremities; slow healing of bones; osteoporosis; back and joint pain; hypertension; decreased immune system resulting in increased risk of infection; thin skin ("steroid skin"); hyperglycemia; increased Na and decreased K* *ACTH stimulation test reveals increased cortisol levels* *Treatment includes: preventing further fluid retention/overload and pulmonary edema; prevention of skin breakdown (turn as tolerated), monitor I&O, daily weights; low sodium, low carb, low protein diet; hand washing; meds= cyprohetadine (Periactin); adrenalectomy or hypophysectomy* *If patient has complete adrenalectomy they will be on lifelong steroid replacement due to removal of adrenal tumor; if hypophysectomy (removal of pituitary) is performed, patient will need to be monitored for CSF leakage; this patient will also be on lifelong steroid replacement*

Cirrhosis

Extensive, non-reversible scarring of the liver -Usually caused by a chronic reaction to hepatic inflammation and necrosis -Develops slowly and results in end-stage liver disease (usually takes decades to develop- although alcohol in combination with Hep C speeds the process up) -Most common causes are Hep C (leading cause in US), alcoholism, and biliary obstruction; worldwide, Hep B and D are leading causes -Without a liver transplant, usually fatal -Some patients have no symptoms until serious complications occur -Impaired liver function results in elevated liver enzymes, portal hypertension, ascities and esophageal varicies, coagulation deficits, jaundice, portal-systemic encephalopathy (PSE) with hepatic coma, hepatorenal syndrome, spontaneous bacterial peritonitis

Care of patient with Alopecia

Hair loss may occur as whole body or may be as mild as thinning on the scalp -Reassure patients that the hair loss is temporary and hair regrowth usually begins about 1 month after completion of chemo -No known treatment prevents alopecia -The priority interventions for the patient with alopecia are to teach injury prevention to the scalp and to assist in coping with this body image change -The hairless scalp is at risk for injury- teach patient to avoid direct sunlight by wearing hats and sunscreen -Items that rub the head can damage the skin; teach patient to wear head coverings under these items -Head coverings are also needed during cold weather to prevent hypothermia

Liver Transplant

Has become a common procedure worldwide -The most common reason for transplant is Hep C -Has become the most effective treatment for an increasing number of patients with acute and chronic liver diseases -Donor livers are obtained primarily from trauma victims who have not had liver damage -The diseased liver is removed and the new liver is attached to the patient's blood vessels and bile ducts -Living donors have also been used and are usually close family members or a spouse -Although liver transplantations are commonly done, complications can occur -Some problems can be medically managed, while others require removal of the transplant -The two most common complications are acute graft rejection and infection -Cyclosporine and many other anti-rejection drugs have improved the success rate greatly -Acute graft rejection occurs 4-10 days after the transplant; manifestations include: tachycardia, fever, RUQ pain, diminished bile drainage or change in bile color or increased jaundice, elevated bilirubin, ALP and prolonged PT -Treated aggressively with immunosuppressive drugs -Infection can occur anytime during recovery; Manifestations include: fever, foul-smelling drainage, tachycardia -Other problems include: bile leakage, abscess formation, hepatic thrombosis, ARF (caused by hypotension, antibiotics, cyclosporine, hypothermia, acute liver failure- watch for early indicators such as decreased urine output)

Causes of shock

Hypovolemic: hemorrhage d/t trauma, GI ulcer, surgery; inadequate clotting d/t hemophilia, liver disease, malnutrition, bone marrow suppression, cancer, anticoagulation therapy; dehydration d/t vomiting, diarrhea, heavy diaphoresis, diuretic therapy, NG suction, diabetes insipidus; hyperglycemia Cardiogenic: MI; ventricular dysrhythmias d/t fibrillation, tachycardia; cardiac amyloidosis ; cardiomyopathies (viral/toxic); myocardial degeneration Distributive: (neural) pain; anesthesia; stress; spinal cord injury; head trauma; (chemical) anaphylaxis; sepsis; capillary leak d/t burns, extensive trauma, liver impairment, hypoproteinemia Obstructive: cardiac tamponade (beck's triad: muffled heart tones, hypotension and JVD), arterial stenosis, pulmonary embolus, pulmonary hypertension, constrictive pericarditis, thoracic tumors, tension pneumothorax

Biliary obstruction

In patients with cirrhosis, the production of bile in the liver is decreased- this prevents the absorption of fat-soluble vitamins such as vitamin K -Without vitamin K, certain clotting factors are not produced in sufficient quantities, and the patient is susceptible to bleeding and easy bruising *-Jaundice* in patients with cirrhosis is caused by either hepatocellular disease or intrahepatic obstruction; hepatocellular jaundice develops because the liver cells cannot effectively secrete bilirubin- this decreased excretion results in excessive circulating bilirubin levels; intrahepatic obstructive jaundice results from edema, fibrosis, or scarring of the hepatic bile channels and bile ducts which interferes with normal bile and bilirubin excretion; patients with jaundice often report pruritis

Tumor lysis syndrome

In tumor lysis syndrome (TLS), large numbers of tumor cells are destroyed rapidly; their intracellular contents, including potassium and purines are released into the circulation faster than the body can eliminate them -Unlike other oncologic emergencies, TLS is a positive sign that cancer treatment is effective -Severe or untreated TLS can cause tissue damage and death; Serum potassium levels can increase to hyperkalemia, causing cardiac dysfunction; the large amounts of purines form uric acid which causes hyperuricemia; these uric acid crystals precipitate in the kidneys, blocking kidney tubules and leading to AKI -TLS is usually seen in patients receiving radiation or chemo for cancers that are very sensitive to these treatments such as: leukemia, lymphoma, small cell lung cancer, and multiple myeloma -Hydration prevents and manages TLS by diluting the K level and increasing kidney filtration/flow; these actions prevent precipitation of uric acid crystals, increase excretion of K, and flush any precipitate -Instruct patients to drink at least 3000-5000 ml of fluid the day before, the day of, and for 3 days after treatment; some fluids should be alkaline to prevent uric acid precipitation; stress the importance of keeping fluid intake consistent and help patients with a schedule -Because patients may have N/V after therapy and may not want to drink fluids, stress the importance of keeping up with antiemetic regimen; instruct pt. to contact the clinic immediately if N/V interferes with adequate fluid intake so that parenteral fluids may be administered -Management is more aggressive for hyperkalemic or hyperuricemic patients; in addition to fluids, diuretics (especially osmotic types) are given to increase urine flow through the kidney; drugs that promote purine excretion such as allopurinol are given; polystyrene sulfate (kayexalate) may be given for moderate hyperkalemia and IV infusions of glucose and insulin may be given for more severe hyperkalemia; patients with severe hyperkalemia/uricemia may need dialysis

Hyperaldosteronism

Increased secretion of aldosterone with mineralcorticoid excess -Increased aldosterone levels affect the kidney tubules and cause sodium retention with potassium and hydrogen ion excretion; Hypernatremia, hypokalemia, and metabolic alkalosis result -Sodium retention increases blood volume which raises blood pressure, but usually does not cause peripheral edema; The elevated blood pressure may cause strokes, heart attacks, and kidney damage *Signs and symptoms include: elevated sodium, decreased K, metabolic alkalosis, fluid overload, headache, fatigue, muscle weakness; hypertension; nocturia, polydipsia, and parathesias (if hypokalemia is severe)* *Surgery (adrenalectomy) is the most common treatment, but patient's potassium levels must be normal; Drugs used to increase potassium levels are spironolactone (Aldactone)- a potassium sparing diuretic and aldosterone antagonist; Potassium supplements may be prescribed to increase potassium levels before surgery; low sodium diet may be prescribed before surgery, but should not be needed after surgery* *Spironolactone may cause hyperkalemia; monitor potassium levels and for dysrhythmias (monitor EKG); monitor patient for fluid overload (crackles, HTN, fluid status, daily weights, headache, fatigue, muscle weakness)*

Hemodynamic monitoring

Indwelling catheter that provides information about blood volume, perfusion, fluid status, and how well heart is pumping; usually performed for more seriously ill patients -Placed through the jugular or subclavian into the right atrium, through the right ventricle into the pulmonary artery and stops; a balloon at the tip is deflated upon entry to the pulmonary artery -Several measurements are taken including: central venous pressure (CVP), pulmonary artery pressure (PAP), pulmonary artery wedge pressure, and cardiac output -Indicated for unstable cardiac client, heart failure, post coronary artery bypass graft, MI, burns and renal failure (volume status) -Central venous pressure in right atrium (CVP) measures right sided venous return (volume)/ preload -Pulmonary arterial pressure (PAP) (lung!) measures pulmonary vascular resistance in the right heart and systemic vascular resistance in the left heart/afterload=resistance; blood shunts to the core (due to vasoconstriction) *-Pulmonary wedge pressure(PAWP) is very important- blocks flow of blood for a second and takes reading; indicates left ventricular function/end diastolic pressure* -Complications include: pneumothorax upon insertion with subclavian entry; infection at site; dysrhythmias (heart reacts-gets irritable when a catheter is put in); embolism (heparinized catheter should prevent this) *-Chest x-ray is always performed post-insertion to confirm proper placement and rule out pneumothorax- you can't do anything until we confirm placement!*; we also listen to lung sounds to assess -Don't forget, informed consent!

Meningitis

Inflammation of the meninges that surround the brain and spinal cord -Viral meningitis is usually self limiting with complete recovery; Bacterial meningitis (meningococcal meningitis) is potentially life threatening -The organisms responsible for meningitis enter the CNS via the bloodstream at the blood-brain barrier; the most frequent organisms responsible for bacterial meningitis are streptococcus pneumoniae (pneumococcal disease) *Signs and symptoms include fever, headache, altered mental status, photophobia, IICP, nuchal rigidity (stiff neck), potistive Kernig's and Brudzinski's signs; seizures; dilated pupils is a late sign of IICP; water retention; red macular rash; decreased LOC* -With symptoms of meningitis, always assume the worst and start patient on broad spectrum ASAP- even before cultures (to wait 3 days for C&S result is too long, and may be too late) -Left untreated, IICP can lead to herniation of the brain and death -Seizure activity may occur and excessive amounts of ADH leads to water retention and SIADH which further increases ICP -The most important nursing action for patients with meningitis is accurately monitoring and documenting their neuro status *The most significant lab test used in diagnosis is the analysis of CSF withdrawn by lumbar puncture; the CSF will look cloudy if bacterial meningitis is present and glucose levels will be decreased; have the client void before puncture, place client in fetal position for puncture and lay flat after; monitor for CSF leak and report any yellow color*

Cirrhosis labs and diagnostics

Labs: -Increased ALT, AST, and LDH (ALT is more specific to the liver; AST can be found in the muscle, kidney, brain, and heart -Increased bilirubin -Protein and albumin are decreased as a result of decreased synthesis by the liver -PT-INR is prolonged (high) -Platelet count is low (thrombocytopenia) -Decreased WBC -Increased ammonia -Low serum sodium -BNP for fluid overload which may cause heart failure Diagnostics: -Labs (AST, ALT, ammonia, albumin, bilirubin, coagulation studies, hepatitis panel) -Hepatic ultrasound (usually first assessment for a person w/suspected liver disease to detect ascites, hepatomegaly, and splenomegaly) -MRI -CT Scan -Biopsy (can be problematic due to bleeding) -EGD for esophageal varacies -ERCP (with contrast dye to allow for stone removals) -Paracentesis -Abdominal x-ray

Pancreatic cancer

Leading cause of cancer deaths each year in the US -Difficult to diagnose early because the pancreas is hidden and surrounded by other organs -Treatment has limited results and 5-year survival rates are low -Tumor may be a primary cancer or result from metastasis from lung, breast, thyroid, kidney, or skin -One of the first signs is jaundice which results from tumor compression and obstruction of bile duct, causing the organ to enlarge; indicates advanced disease state -Metastasis to the liver may cause hepatomegaly -Regardless of where it originates, it spreads rapidly through the lymphatic and venous systems to other organ -Venous thromboembolism is a common complication of pancreatic cancer; necrotic products of the tumor are believed to have thromboplastic properties -Smoking and age are the highest risk factors followed by DM, chronic pancreatitis, cirrhosis, high intake of red meat and processed meats; long term exposure to chemicals, and obesity -The most common concern is fatigue; the patient notices an inability to perform usual physical or intellectual activities -Other key features include: jaundice, clay colored stools, dark urine, abdominal pain (usually vague, dull, or nonspecific and radiates to the back); weight loss; anorexia; nausea or vomiting; glucose intolerance; splenomegaly; flatulence; GI bleed; ascities; leg or calf pain (DVT) -No specific blood tests diagnose pancreatic cancer, but amylase, lipase, alp and bilirubin levels are increased; abdominal US and CT confirm tumors

Hypovolemic shock

Loss of blood volume from the vascular space causes a decreased MAP and a loss of oxygen carrying capacity from the loss of RBCs; Reduced MAP slows blood flow, resulting in decreased tissue perfusion -The main trigger leading to hypovolemic shock is a sustained decrease in MAP -A decrease in MAP of 5-10 mm Hg below pt's normal baseline is detected by baroreceptors and triggers compensatory mechanisms that help ensure continued blood flow to vital organs while reducing blood flow to less vital areas (shunting)- this process results in some shock manifestations -If the events that cause the decreased MAP are halted at this stage, compensatory mechanisms provide adequate perfusion w/o outside intervention; if the events continue, however, and MAP decreases further, some tissues function under anaerobic conditions which increases lactic acid levels and other harmful metabolites (these substances cause electrolyte and acid-base imbalances with tissue damaging effects and depressed heart muscle activity -These effects are temporary and reversible if shock is corrected within 1-2 hours after onset; when shock conditions continue for longer periods w/o help, the resulting acid-base and electrolyte imbalance and metabolites cause so much cell damage in vital organs that MODS occurs and recovery from shock is not longer possible

Types of Shock

More than one type of shock can be present at the same time (e.g. trauma caused by a car crash may trigger hemorrhage leading to hypovolemic shock and a MI leading to cardiogenic shock) -Hypovolemic shock occurs when too little circulating blood volume causes a MAP decrease, resulting in inadequate total body oxygenation; common problems leading to hypovolemic shock are hemorrhage and dehydration -Cardiogenic shock occurs when the actual heart muscle is unhealthy and pumping is directly impaired; MI is the most common cause of direct pump failure; Any type of pump failure decreases cardiac output and MAP -Distributive shock occurs when blood volume is not lost from the body but is distributed to the interstitial tissues where it cannot circulate to deliver oxygen; it can be caused by lack of sympathetic tone, blood vessel dilation, pooling of blood in capillary beds, and increased capillary leak; all these factors can decrease MAP and may be started by nerve damages (neural shock that occurs when sympathtic nerve function decreases- sympathetic tone) or by chemicals (anaphylactic shock, septic shock, and capillary leak syndrome) in the blood that start widespread changes in the blood vessel walls -Obstructive shock is caused by problems that impair the ability of the (otherwise normal) heart muscle to pump effectively; the heart itself remains normal, but conditions outside the heart prevent either adequate filling of the heart or adequate contraction of the heart muscle; the most common causes of obstructive shock are pericarditis and cardiac tamponade -Although the causes and initial mechanisms associated with the different types of shock vary, eventually the side effects of hypotension (anaerobic cellular metabolism) result in the common key features of shock

Care of patient with Mucositis

Mucositis (sores in the mucous membranes) often develops in the entire GI tract, especially the mouth (stomatitis) -Frequent mouth assessment and oral hygiene are key in managing stomatitis and mucositis -Stress the importance of good and frequent oral hygiene, including teeth cleaning and oral rinsing -Because most patients with mucositis also have myelosuppression, they must take care to avoid traumatizing the oral mucosa -Soft bristled toothbrushes for toothbrushing every 8 hours, disposable mouth sponges and gentle flossing once daily should be taught -Mouthwashes with alcohol or other drying agents should be avoided; rinse mouth with one normal saline/one half peroxide every 12 hours and 4 times daily with a bland rinse -Drink 2 or more liters of water a day -Avoid spicy, hard, acidic, dry or rough foods and hot liquids -Mouth should be inspected every 4 hours for fissures, blisters, sores, or drainage -Oral hygiene equipment should be kept clean; patients should clean toothbrushes weekly in a dishwasher with bleach or hydrogen peroxide -Many compounds are available for pain relief from stomatitis that contain local anesthetics and anti-inflammatory agents

Hepatitis D

Occurs only with Hep B virus as a helper virus for replication -Incubation is 14-56 days -Transmitted parenterally, especially in IV drug abusers -Having sex with an infected person is also a high risk factor

Nonprogressive stage of shock (compensatory)

Occurs when MAP decreases by 10-15 mm Hg from baseline -Kidney and hormonal compensatory mechanisms are activated because cardiovascular responses alone are not enough to maintain MAP -Kidneys and baroreceptors respond by triggering release of renin, ADH, aldosterone, epinephrine and norepinephrine to start kidney compensation; these compensatory mechanisms maintain fluid volume within central blood vessels -Tissue hypoxia occurs in nonvital organs (skin, GI tract, etc.) and in the kidney, but it is not enough to cause permanent damage -Acid-base and electrolyte changes occur such as acidosis and hyperkalemia -Manifestations include both subjective and objective changes reulting from decreased tissue perfusion; subjective changes include increased thirst and anxiety; objective changes include restlessness, tachycardia, increased RR, decreased UO, falling systolic BP, rising diastolic BP, narrowing pulse pressure, cool extremities, and a 2%-5% decrease in O2 sat -Comparing these changes with the values and manifestations obtained earlier is critical to identifying this stage of shock -If the patient is stable and compensatory mechanisms are supported by interventions, the pt can stay in this stage for hours without permanent damage -Stopping the condition that started the shock at this time and providing supportive interventions can prevent the shock from progressing; the cellular effects of this stage are reversible when nurses recognize the problem and coordinate w/the health care team to start interventions -Interventions include: finding the source, aggressive resuscitation of fluids (watch lung sounds, we don't want to drown them); oxygen/intubate; antibiotics within one hour; labs (should see increased lactic acid, change in WBC- up or down; acidosis- high PaCO2/low PaO2; hyperkalemia)

Progressive shock (intermediate)

Occurs when there is a sustained decrease in MAP of more than 20 mm Hg from baseline -In this stage, compensatory mechanisms are functioning, but can no longer deliver sufficient oxygen, even to vital organs; the heart uses even more oxygen than normal thus increasing the demand further -Vital organs develop hypoxia, and less vital organs become anoxic and ischemic (the liver is the first to go, but we will see evidence from the kidneys first- no BP, no PP) -As a result of poor oxygenation and a buildup of toxic metabolites, some tissues have severe cell damage and die -Manifestations of the progressive stage include a worsening of subjective and objective changes r/t decreased tissue perfusion -Continous monitoring and comparison w/ earlier findings are critical to assess therapy effectiveness -Subjective changes include: severe thirst sensation and deepening anxiety; the patient may express impending doom (i'm gonna die); pt. may seem confused/ altered LOC -Objective changes include: rapid, weak pulse; low BP; pallor to cyanosis of oral mucosa and nail beds; cool, moist skin; anuria; and a 5-20% decrease in O2 sat -Labs at this stage reveal: low blood pH, along with rising lactic acid and potassium levels -The progressive stage of shock is a life-threatening emergency; vital organs can tolerate this situation for only a short period of time before being damaged permanently; immediate interventions are needed to reverse the effects of this stage of shock; tolerance varies from person to person and depends on age and health -The patient's life can usually be saved if the conditions causing shock are corrected within 1 hour or less of the onset of the progressive stage

Refractory stage of shock (Irreversible)

Occurs when too much cell death and tissue damage result from too little oxygen reaching the tissues -Vital organs have overwhelming damage and the body can no longer respond effectively to interventions-shock continues -Anaerobic metabolism occurs causing acidosis -Therapy is not effective in saving the patient's life, even if the cause of shock is corrected and MAP temporarily returns to normal -So much tissue damage has occurred with widespread release of toxic metabolites and enzymes that cell damage in vital organs continues despite aggressive interventions -Patient will present with: rapid loss of consciousness, nonpalpable pulse, cold and dusky extremities; slow, shallow breathing, and unmeasurable O2 sat -Patient will die

Reperfusion therapy

Opens an occluded artery by medication or mechanical means -Includes fibrinolytics/thrombolytics (medical) or Percutaneous coronary interventions (mechanical) -Thrombolytic therapy using fibrinolytics dissolves thrombi in the coronary arteries and restores myocardial blood flow; examples include t-PA, alteplase, streptokinase, reteplase, or tenecteplase (big one we use); thrombolytic agents are *most effective when administered within first 6 hours* of a coronary event; the patient must be continuously monitored for bleeding

Oxygenation and tissue perfusion

Oxygenation and tissue perfusion depend on how much oxygen from arterial blood perfuses to the tissue -Total blood volume and cardiac output are directly related to the mean arterial pressure (MAP), so increases in either total blood volume or cardiac output RAISE MAP and decreases in either total blood volume or cardiac output LOWER MAP -The size of the vascular bed is inversely r/t MAP; this means that increases in the size of the vascular bed DECREASES MAP and decreases in the size of the vascular bed INCREASES MAP -When blood vessels dilate but blood volume stays the same, the blood pressure will drop and the blood flow will become slower; this means your patient is getting less oxygen to the tissues and is becoming hypoxic

Pulseless Electical Activity

PEA -The absence of a palpable pulse and myocardial muscle activity with *the presence of organized electrical activity EXCLUDING Vtach, Vfib, and Asystole on the monitor* -It is not an actual rhythm and *actually represents a clinical conditon wherein the client is clinically dead despite the fact that some time of organized rhythm appears on the monitor* -The heart is pumping, but it is too faint to generate a pulse *Priority is to find and treat the cause!* *-Most commonly caused by hypovolemia and/or hypoxia*; "H's and T's: hypovolemia, hypoxia, hydrogen ions (acidosis), hypothermia, hyper/hypokalemia, hypoglycemia; Tablets or Toxins (drug overdose), tamponade, tension pneumothorax, thrombosis (MI), thrombosis (PE which causes hypovolemia/hypoxia) -Treatment: *Find and treat the cause while doing CPR immediately; if the question asks "what do we do for the best patient outcome"- the answer is "find and treat the cause"; if the question asks "what is our priority action?"- the answer is CPR!*; Epi 1 mg Q3-5 min, Vasopressin 40 units IVP; Other meds depending on the cause (fluids for hypovolemia, K for hypokalemia, etc.); research no longer supports use of atropine; sodium bicarb may be used if known acidosis but there is little evidence to support its effectiveness; *DO NOT DEFIBRILLATE*

Premature Ventricular contractions

PVCs -Result from increased irritability of ventricular cells and are seen as early ventricular complexes followed by a compensatory pause *-Premature beat is usually "wide and bizarre" in appearance* -PVCs are common and their frequency increases with age; they may be insignificant, or may occur with problems such as MI, CHF, COPD and anemia -PVCs may also be present with hypokalemia or hypomagnesemia -Sympathomimetic agents such as anesthesia, drugs, stress, nicotine, caffeine, alcohol, infection or surgery can also cause PVCs-especially in older adults -The patient may be asymptomatic or experience palpations or chest discomfort caused by increased stroke volume of the normal beat after the pause -Peripheral pulses may be decreased or absent with the PVCs themselves because the decreased stroke volume of the premature beats may decrease peripheral perfusion; *because other dysrhythmias can cause widened QRS complexes, assess whether the premature complexes perfuse to the etremities; palpate the carotid, brachial, or femoral arteries while observing the monitor for widened complexes or auscultating heart sounds; with acute MI, PVCs may be considered a warning, possibly triggering life-threatening vtach or vfib* -If there are no underlying heart diseases, we treat and eliminate the cause (usually hypokalemia, caffeine, digoxin, nicotine, stress) -People with more than 5000 PVCs in a 24 hour period are usually given beta blockers -In the presence of heart disease (MI), we must monitor for Vtach, Vfib, administer antidysrhythmics (amiodarone or lidocaine)

SIADH

Problem in which vasopressin (ADH) is secreted even when plasma osmolarity is low or normal -Leads to renal reabsorption of water and causes excretion of sodium leading to *water intoxication*, cellular edema, and dilutional hyponatremia *Signs and symptoms include oliguria (less than 400/day; decreased appetite, N/V, diarrhea, weight gain, weakness, hyponatremia; concentrated urine and decreased serum osmolarity* *Treatment includes: fluid restriction (500-600ml/day); lasix- if sodium levels are near normal; for milder SIADH, declomycin (oral antibiotic) may be given- watch for oral candiasis; hypertonic fluid (3% saline) depending on Na level- if only slightly low, may not need this much sodium* *Complications include: fluid overload (AEB decreased osmolarity) and pulmonary edema (listen to lung sounds, monitor for jvd, bounding pulse and decreased urine output; monitor daily weights- a weight gain of 2 lbs or more/day or gradual increase over several days is cause for concern); water intoxication (headache, acute confusion); seizures (if Na falls below 120- monitor neuro status and provide safe environment)*

Parkinsons Disease

Progressive neurodegenerative disease that is one of the most common neurologic disorders of older adults -It is a debilitating disease affecting motor ability and is characterized by four cardinal symptoms: tremor, rigidity, bradykinesia or akinesia (slow/no movement) and postural instability -Decreased levels of dopamine in the brain causes the patient to lose the ability to refine voluntary movement -Parkinsons also causes the reduction of sympathetic nervous system influence on heart and blood vessels resulting in orthostatic hypotension *Signs and symptoms include: slow and shuffling gait, stooped posture, short, hesitant steps, bradykinesia, tremors, pill rolling movement, difficulty swallowing and chewing, uncontrolled drooling, masklike facies (wide open, fixed, staring eyes), emotional lability, oily skin, paranoia, mood swings, dysarthria, echolalia, hypophonia* -Bowel and bladder problems such as urinary incontinence and constipation can occur due to malfunction of the autnomic nervous system -*Treatment is supportive; drugs are prescribed to increase patient's functional abilities and quality of life; dopamine agonists, anticonvulsants, anticholinergics; Safety is priority- patient is at risk for falls and aspiration; ensure fall risk precautions are in place and thickeners are added to liquids as well as food cut into small bites; stay close to patients with blurry vision*

Chronic pancreatitis

Progressive, destructive disease of the pancreas that has remissions and exacerbations (flare ups) -Inflammation and fibrosis of the tissue contribute to pancreatic insufficiency and diminished function of the organ -Most common type is chronic calcifying pancreatitis and alcoholism is the primary risk factor -Pancreatic insufficiency in any type of chronic pancreatitis causes loss of exocrine function; most patients have decreased pancreatic secretions and bicarbonate; steatorrhea may result from severe malabsorption of fats causing pale, bulky, foul smelling, frothy stools -Fat malabsorption also leads to weight loss and muscle wasting; protein malabsorption leads to "starvation edema" of the feet legs, and hands caused by decreased albumin -Loss of endocrine function results in diabetes mellitus -Pulmonary complications such as ARDS may develop

Metabolic syndrome (syndrome x)

Recognized as a risk factor for cardiovascular disease and is being aggressively researched -Patients who have three of the following factors are diagnosed with metabolic syndrome: hypertension (130/85 or higher), decreased hdl less than 40-50 (usually with high ldl), increased level of triglycerides (150 or higher), increased FBG of 100 mg/dl or higher (diabetes, etc.), large waist size (40 inches or greater for men/ 35 inches or greater for women)

Cholecystitis (Chronic)

Results when repeated episodes of cystic duct obstruction cause chronic inflammation -Calculi are almost always present; the gallbladder becomes fibrotic and contracted, which results in decreased motility and deficient absorption -Pancreatitis and cholangitis (bile duct inflammation) can occur as chronic complications of cholecystitis; these result from the backup of bile through the biliary tract; bile obstruction leads to jaundice -Jaundice may occur in patient with acute cholecystitis but is most commonly seen in those with the chronic form -Accumulation of bile salts in the skin causes pruritis or a burning sensation -Patient will present with possible chest pain, pain in between shoulder blades, GI upset, feeling of fullness, gas, belching, etc. -Patients may have slowly developing symptoms and may not seek medical treatment until late symptoms such as jaundice, clay colored stools, and dark urine occur; Icterus (yellowing of the sclerae and oral mucous membranes) may also be present; Seatorrhea (fatty stools) may occur due to decreased fat absorption from lack of bile; Patient may have an elevated temp, tachycardia, and dehydration from fever and vomiting

Sepsis and Septic shock

Sepsis and septic shock is a complex type of distributive shock that usually begins as a bacterial or fungal infection and progresses to a dangerous condition over a period of days -*As progression occurs, the pathologic problems occur faster and to a greater degree; thus control of sepsis and prevention of severe sepsis and septic shock through appropriate interventions are easier to achieve early in the course of the problem; failure to recognize and intervene in early sepsis is the major cause of progression to septic shock and death* -Sepsis is a condition in which infectious organisms have entered the bloodstream; as the numbers grow in the bloodstream, an inflammatory response known as Systemic Inflammatory Response Syndrome (SIRS) is triggered and as a result, leads to extensive hormonal, tissue, and vascular changes and oxidative stress that further impairs oxygenation and tissue perfusion -Widespread vasodilation and subsequent blood pooling occurs; the patient has mild hypotension, increased RR, and low to high grade fever; Usually at this stage, the patient has elevated WBCs -Microthrombi begin to form in some organ capillaries causing hypoxia and reducing organ function; this problem is hard to detect, but if sepsis is stopped at this point, the organ damage is completely reversible; the microthrombi increase hypoxic conditions which then generate more toxic metabolites- those damage more cells and increase inflammation leading to an amplification of SIRS and a vicious repeating cycle of poor oxygenation/tissue perfusion -Although these manifestations are subtle, they indicate sepsis and SIRS and will progress unless interventions begin now; when SIRS and sepsis is not identified at this stage, it almost always progresses to severe sepsis, which is much harder to control; identifying criteria by the facility must be used to ensure intervention -Notify the health care provider or rapid response for any patient who has vital signs or other conditions that meet the sepsis with SIRS criteria

Spinal cord injury

Spinal cord injuries involve *loss of: motor function, sensory function, reflex activity, bowel and bladder control* -Most trauma to the spinal cord causes permanent disability or loss of movement (paralysis) and *sensation below the site of the injury* Intervention at the scene includes: ABCs, Vitals, Glasgow Coma Score, *Neck/Spine stabilization-priority!*; Maintaining BP; multisystem support, GI assessment *Treatment goal is to prevent further injury; prevent neurogenic shock, spinal shock, and autonomic dysreflexia* *Neurogenic shock occurs in acute stage of spinal cord injury; usually in injuries above T6; Interruption of the CNS causes disruption of sympathetic outflow causing a decreased heart rate and blood pressure; signs and symptoms include: warm and dry skin, hypotension, bradycardia, hypothermia; Treatment includes: FLUIDS!, dopamine, vasopressors* *Spinal shock causes immediate and temporary loss of motor, sensory, reflex, and autonomic function; usually lasts less than 48 hours to a few weeks; causes temporary paralysis, loss of sensation, loss of b & b control; Spasticity or hyperreflexia signals the end of this shock* *Major complication is autonomic dysreflexia= below T6 intact sensory nerves transmit impulses up the spinal cord BUT, sympathetic inhibitory impulses are blocked; epi and norepi are released; patient has hypertension; Most common cause of noxious stimuli is distention of the bowel or bladder caused by urinary retention or constipation; simple kinks in tubing of catheter can trigger this; If client has high BP, complains of headache, etc., check urinary output- make sure cath is draining, may need to straight cath; palpate bladder using Crede's method but be careful not to palpate too hard- this can worsen HTN; Give stool softeners, laxatives or manual extraction for abdominal distention*

Hepatitis B

Spread through unprotected sex, sharing needles, accidental needle sticks, unscreened blood transfusions, hemodialysis, maternal-fetal route, close person to person contact with open cuts and sores -Most of us are vaccinated against it -Symptoms usually occur within 25 to 180 days of exposure and usually include: anorexia, nausea, vomiting; fever, fatigue; right upper quadrant pain; dark urine with light stool; joint pain and jaundice -Blood test confirms, though many people have no symptoms -Most adults recover and develop immunity, however, a small percentage of people become carriers and can infect others; chronic carriers are at high risk for cirrhosis and liver cancer

Superior Vena Cava syndrome

Superior vena cava (SVC) syndrome occurs when the SVC is compressed or obstructed by tumor growth or clots in the vessel SVC compression is painful and life threatening and occurs in most patients with lymphomas, lung and breast cancer -The manifestations result from the blockage of venous return from the head, neck, and upper trunk -Early manifestations arise after a night's sleep and include edema of the face, especially around the eyes, and tightness of the shirt or blouse collar -As the compression worsens, the patient develops engorged blood vessels and erythema of the upper body, edema in the arms and hands, dyspnea and epistaxis -Late manifestations include hemorrhage, cyanosis, mental status changes, decreased cardiac output, and hypotension -Death results if compression is not relieved -SVC syndrome is a late-stage manifestation; the tumor is usually widespread -High dose radiation therapy to the upper chest area may be used to provide temporary relief; surgery is rarely performed for this condition -A metal stent can be placed in the vena cava in an interventional radiation department to relieve swelling; follow up angioplasty can keep this stent open for a longer period

Cancer staging

The TNM system is used to describe the general anatomic extent of cancers; the stages guide treatment and are useful for prognosis and comparison of treatment results -TNM staging systems have specific prognostic value for each solid tumor type -TNM is not useful for leukemia or lymphoma -The TNM system is based on the size and or extent/reach of the primary tumor (T), the amount of spread to nearby lymph nodes (N), and the presence of metastasis (M) or secondary tumors; a number is added to each letter to indicate size and/or extent of the primary tumor and degree of cancer spread -Primary Tumor (T): Tx: Primary tumor cannot be assessed; T0: No evidence of primary tumor; Tis: Carcinoma in situ; T1, 2, 3, 4: Increasing size and/or local extent of the primary tumor -Regional Lymph Nodes (N): Nx: Regional lymph nodes cannot be assessed; N0: No regional lymph node metastasis; N1, 2, 3: Increasing involvement of regional lymph nodes -Distant Metastasis (M): Mx: Presence of distant metastasis cannot be assessed; M0: No distant metastasis; M1: Distant metastasis

Hepatorenal syndrome (HRS)

The development of hepatorenal syndrome indicates a poor prognosis for the patient with liver failure -It is often the cause of death in these patients and is manifested by: sudden decrease in urinary output (less than 500 ml/24 hours- oliguria); Elevated BUN and creatinine w/ abnormally decreased urine sodium excretion; Increased urine osmolality -Often occurs after a GI bleed or onset of PSE -Patients with cirrhosis and ascites may develop *acute spontaneous bacterial peritonitis (SBP)* -Clinical manifestations may include: fever, chills, and abdominal pain/tenderness although manifestations may also be minimal with only mild symptoms with absence of fever -Worsening encephalopathy and increased jaundice may also be present without abdominal symptoms -Diagnosis of SBP is made when fluid obtained by parecentesis has a leukocyte count of more than 250

Chronic Pancreatitis Treatment

The focus of caring for a patient with chronic pancreatitis is pain management, nutritional balance, and prevention of recurrence -Pancreatic enzyme replacement therapy (PERT) is the standard of care for malnutriton, malabsorption, and excessive weight loss (Pancrealipase); the dosage depends on the severity of malabsorption; record number and consistency of stools per day to monitor effectiveness of treatment (i.e., stools should become less frequent and less fatty) -Teach patient who is taking PERT to take these drugs with meals and snacks and a glass of water and should swallow whole; patients who have difficulty swallowing should cover capsules with applesauce or open them and spread them over mashed foods; PERT should not be mixed with foods containing proteins because the enzymes will break them down and turn them into a watery substance; be sure patients drink a full glass of water after taking drug to make sure none of the enzymes remain in the mouth; advise patients to wet their lips with a wet towel to prevent skin irritation and breakdown that residual enzymes cause; Administer enzymes after antacids or H2 blockers (enzymes inactivate these drugs); follow up on labs- pancrealipase can cause an increase in uric acid levels -If the patient has diabetes, they will be prescribed insulin for glucose control (watch patients on TPN; check FSBG Q 2-4 H) -Nutritional interventions are similar as with acute pancreatitis; if the patient is avoiding food to reduce pain, TPN or TEN may be administered; long term dietary management may require an increased caloric intake to equal 4000-6000 calories/day; foods high in protein and carbs assist the healing process; avoid fats and alcohol -Teach patient to avoid alcohol and nicotine and to eat small meals and snacks high in protein; restrict activity until strength is regained- rest frequently -Chronic pancreatitis patient has a higher risk for pancreatic cancer

Side effects of radiation therapy

The immediate and long term side effects of all types of radiation are limited to the tissues exposed to the radiation, therefore the side effects vary according to the site -Skin changes and hair loss are local but often permanent depending on the total absorbed dose -Altered taste sensations and fatigue are two common systemic side effects noted by patients receiving teletherapy regardless of radiation site -Regardless of the cause, radiation-induced fatigue can be debilitating and last for months -Radiation damage to normal tissues during cancer therapy can start inflammatory processes that lead to tissue fibrosis and scarring; these effects may appear years after radiation treatment -Teaching patients about skin care needs is a priority intervention; Teach patients to wash the irridated area each day with water and mild soap and not to remove any ink markings; Teach patient to dry area with patting rather than rubbing motions; use only oncology approved lotions, creams or powders; wear soft clothing over site and avoid any binding materials over site as well as exposure to the sun and heat -Radiation to the head/throat and upper chest can lead to difficulty swallowing and dry mouth. Nutritionists and strict dental care should be adhered to in order to maintain balanced nutrition and prevent tooth decay

Liver Trauma

The liver is one of the most common organs to be injured in patients with abdominal trauma -Damage or injury should be suspected whenever any upper abdominal or lower chest trauma is sustained -The liver is often injured by steering wheels in MVCs -Common injuries include lacerations, tears, and crush injuries -The liver is a highly vascular organ and receives almost a third of the body's cardiac output; When hepatic trauma occurs, blood loss can be massive= *observe for early signs of hypovolemic shock* such as hypotension, tachycardia, tachypnea, pallor, diaphoresis, cool and clammy skin, confusion or change in mental state -Other features include right upper quadrant pain with abdominal tenderness, abdominal distention and rigidity, guarding of the abdomen, increased pain when breathing and referred pain to the right shoulder -Minor surgical interventions are often performed to stop the bleeding; The client may require lots of blood or blood products

Myocardial infarction

The most serious of the acute coronary syndromes -Untreated or undiagnosed angina can lead to this very serious problem -Occurs when myocardial tissue is abruptly and severely deprived of oxygen -Ischemia develops due to lack of blood flow below the level of occlusion and can lead to injury and necrosis of myocardial tissue (due to hypoxia) if blood flow is not restored -Most MIs are the result of atherosclerosis, rupture of the plaque, subsequent thrombosis (body knows it's injured- platelets run to the area and further increase the blockage- this is why we give chewable ASA- works faster), and occlusion -Infarction is a dynamic process that does not occur instantly; it evolves over a period of several hours -Obstruction of the LAD causes anterior or septal MIs which have the highest mortality rate because they are most likely to have left ventricular failure and dysrythmias from damage to the left ventricle -Historically, an acute MI was diagnosed by the presence of ST-segment elevation, however, all patients do not present with this finding, instead, they are classified into one of the three categories according to the presence or absence of ST-segment elevation on the ECG and positive troponin markers: ST-elevation MI (STEMI); Non-ST elevation MI (NSTEMI) (common in women); Unstable angina -Patients presenting with STEMI typically have ST elevation in two contiguous leads on a 12-lead ECG- this indicates myocardial infarction/necrosis and requires immediate treatment *-Majority of deaths from MI occur within 1 hours of symptoms, yet the average time a person seeks treatment is 4 hours- this why we say "time is muscle"* -Research shows improved outcomes following MI in clients treated with ASA (81 or 325 mg when they go home), beta blockers, and ACEs (less oxygen demand); aggressive use of AED in the field is key

Shock treatment

The priority problem for patients with hypovolemic shock are: Hypoxia r/t hypovolemia; Hypoperfusion r/t fluid volume loss and hypotension; Anxiety r/t potential for death and decreased cerebral perfusion; Confusion r/t decreased cerebral perfusion -Oxygen therapy is for any stage of shock -IV therapy for fluid resuscitation is a primary intervention for hypovolemic shock (after establishing airway); crystalloids and colloids are the fluids of choice for replacement; two common solutions are normal saline and ringers lactate (contains sodium, chloride, potassium, and lactate-expands volume and buffers acidosis) *use only normal saline if also infusing blood or blood products (colloids)* -Drug therapy is used when volume lost is severe and the patient does not respond to fluid replacement; the actions of the drug for shock increase venous return, improve cardiac contractility, or improve perfusion by dilating coronary vessels; vasoconstricting drugs such as Dopamine (inotropin) and Norepinephrine (Levophed) increase cardiac ouput; Inotropic drugs ushc as Dobutamine stimulate receptors in the heart and improve contraction; Drugs enhancing myocardial perfusion (nitropress) help ensure the heart is well perfused (monitor patient closely- vasodilation can increase shock if volume is depleted) -Monitoring vitals and LOC are major nursing actions to determine effectiveness of therapy; assess pulse, BP, pulse pressure, CVP, resp. rate, skin and mucosal color, O2 sat, Mental status, urine output; *assess these parameters every 15 minutes until the shock is controlled and patient's condition improves*

Sepsis treatment

The priority problem for patients with septic shock is potential for MODS -Interventions for sepsis and septic shock focus on identifying the problem as early as possible, correcting the conditions causing it, and preventing complications -The use of a sepsis resuscitation bundle for treatment of sepsis is the standard of practice -A bundle is a group of two or more interventions that have been shown to be effective when applied together or in a sequence -Sepsis Resuscitation bundle: 1) measure serum lactate levels; 2) obtain blood cultures (2 sets) BEFORE administering antibiotics; 3) administer broad spectrum antibiotic therapy within 1 hour of establishing a diagnosis; 4) If either hypotension or lactate level greater than 4 is present, administer an IV infusion of 1000 ml crystalloids or 300-500 ml of colloids over 30 minutes; if hypotension does not respond to initial fluid resuscitation by increasing the MAP to at least 65, start IV vasopressor (levophed or dopamine) therapy; 5) If hypotension persists despite fluid resuscitation and vasopressor therapy, and either septic shock is present or the lactate level remains over 4, use these parameters to monitor therapy effectiveness: CVP of at least 8; central venous O2 sat of at least 70% or mixed O2 sat of at least 65% -Sepsis management bundle: 1) When septic shock is present, administer low dose steroids in accordance with ICU protocol; 2) Administer drotrecogin alfa for patients meeting ICU and drotrecogin criteria; 3) Administer insulin to maintain blood glucose at least lower than 150; 4) Use mechanical vent to maintain inspiratory plateau pressures less than 30 -The patient is septic shock is more likely to be mechanically ventilated -Drug therapy includes the same cardiac drugs to restore volume as in hypovolemic shock; vancomycin, aminoglycosides, systemic penicillin, cephalosporins, macrolides, and quinolones; Corticosteroids can support adrenals; insulin therapy to combat increased glucose levels; heparin to limit clotting; synthetic activated protein C; drotrecogin alfa for patients at high risk for death; blood replacement therapy for hemorrhage

Acute Pancreatitis Treatment

The priority problems for patients with acute pancreatitis are: Acute pain r/t inflammation and enzyme leakage and Inadequate nutrition r/t inability to ingest food and absorb nutrients -Mild pancreatitis requires hydration with IV fluids, pain control, and drug therapy -Nonsurgical management includes: fasting and rest, drug therapy, and comfort measures -To rest the pancreas and reduce pancreatic enzyme secretion, withhold food and fluids during the acute period -IV hydration and IV replacement of calcium and magnesium may also be needed (banana bag); measure and document I&O -Prolonged NG intubation may be necessary if paralytic ileus is present- assess bowel sounds frequently for return of peristalisis -Enteral feeding is preferred over TPN because it causes fewer episodes of glucose elevation and other complications -Weigh pt. daily -When food is tolerated in the healing phase, small, frequent, moderate to high carb, high protein, low fat meals can be started; food should be bland and coffee, tea, chocolate, cola, and alcohol should be avoided -Monitor the patient who begins oral intake for nausea, vomiting, and diarrhea- if any of these symptoms occur, notify HCP immediately -PCA pump with morphine or hydromorphone are typically used because demerol can cause seizures; other options are transdermal fentanyl and epidural analgesia -Histamine receptor antagonists (rantidine) and PPIs (omeprazole) help decrease gastric acid secretion -Antibiotics may be used for acute necrotizing pancreatitis -Help pt. assume side lying (fetal) position or sit with knees flexed toward chest to help abdominal pain -Surgical intervention is not usually indicated unless pancreatitis was caused by gallstones -Monitor resp status and for signs of pleural effusion -Observe for signs of hypocalcemia (chvostek's and trousseau's)

Severe sepsis

The progression of sepsis with an amplified inflammatory response; All tissues are involved and hypoxic to some degree -Some organs are experiencing cell death and dysfunction at this time; Microthrombi formation is widespread and using much of the available platelets and clotting factors (DIC) -The continued stress response triggers the continued release of glucose from the liver and causes hyperglycemia; the more severe the response, the higher the blood glucose level -Despite the severity of this stage, it is often missed because patient's cardiac function is hyperdynamic at this stage; patient will have an increased HR and BP and may even look better and WBC may no longer be elevated because they are no longer producing -Clinical manifestations include: lower oxygen sat, rapid RR, decreased to absent urine output, and a change in pt cognition and affect -Appropriate and aggressive interventions at this stage can still prevent septic shock, although mortality after a patient reaches this stage is much higher for sepsis and SIRS -At this point, the downhill course to septic shock is extremely rapid

Multiple Organ Dysfunction Syndrome (MODS)

The sequence of cell damage caused by the massive release of toxic metabolites and enzymes -Once the damage has started, the sequence becomes a vicious cycle as more dead cells break open and release harmful metabolites -Small clots form, which block tissue oxygenation and damage more cells, thus continuing the devastating cycle -Liver, heart, brain, and kidney functions are lost first; the most profound change is damage to the heart muscle

Septic shock

The stage of sepsis and SIRS when multiple organ failure is evident and uncontrolled bleeding occurs -Even with appropriate intervention, the death rate among patients in this stage of sepsis exceeds 50% -Severe hypovolemic shock is present as a result of an inability of blood to clot because platelets and clotting factors have been used up -Capillary leak continues and cardiac contractility is poor from cellular ischemia -Clinical manifestations resemble the late stage of hypovolemic shock

Hepatitis C

Transmission is blood to blood -Biggest Hep virus to worry about these days -Silent killer= can be in system without showing up for many months or years after being infected and may be discovered during a routine lab eval or when liver problems occur -Carriers can infect someone even if they are not sick; the disease is not transmitted by casual contact or by intimate household contact, however, those infected are advised not to share items that may contain blood products on them (toothbrushes, razors, etc.) -Spread most commonly by: illicit IV drug needle sharing (most common); blood, blood products, or organ transplants received before 1992; needle stick injury with contaminated blood; unsanitary tattoo equipment; sharing of intranasal cocaine paraphernalia -Average incubation is 7 weeks though acute infection and illnesses are not common -Most people infected do not clear the virus and a chronic infection develops -Usually does its damage over decades by causing a chronic inflammation that causes the liver cells to scar leading to cirrhosis- alcohol use increases the progression and severity of cirrhosis -Hep C induced cirrhosis is the leading indication for liver transplant in the US, however, the newly transplanted liver often becomes re-infected with the virus (will only buy the patient 5-10 years until they need another transplant)

Cancer grading

Tumor grade is not the same as cancer staging -It is the description of a tumor based on how abnormal the tumor cells look and is an indicator of how quickly it is likely to grow and spread -Grading is needed because some cancer cells are more malignant than others -A well-differentiated tumor tends to grow and spread at a slower rate than an undifferentiated or poorly differentiated tumor which have abnormal looking cells and tissue structure -Based on these and other differences, the tumor is assigned a numerical "grade" Gx= Grade cannot be determined G1= tumor cells are well-differentiated and closely resemble normal cells; considered a low grade of malignant change; malignant but slow growing G2= moderately differentiated; still retain some characteristics of normal cells but also have more malignant characteristics than G1 tumor cells G3= tumor cells are poorly differentiated, but the tissue of origin can usually be established; the cells have few normal cell characteristics G4= Tumor cells are poorly differentiated and retain no normal cell characteristics; determination of the tissue origin is difficult to impossible

Symptoms of cancer

Unexplained weight loss: of 10 lbs or more; happens most often w/ cancers of pancreas, stomach, esophagus or lung Fever: very common but happens more often after cancer has spread/ can also be due to immunosuppresion from treatment Fatigue: extreme tiredness that doesn't get better with rest; may happen early in some cancers like leukemia Pain: may be an early symptom with cancers like bone cancer; Headache that does not go away may be a symptom of a brain tumor; Back pain can be a symptom of colon, rectal or ovarian cancer; Most often, pain due to cancer means it has already spread Skin changes: other than skin cancers, some other cancers can cause skin changes such as hyperpigmentation, jaundice, erythema, pruritis, and excessive hair growth

Ventricular Fibrilation

VFib *-Electrical CHAOS in the ventricles and is life threatening* -Impulses from many irritable foci fire in a totally disorganized manner so that ventricular contraction cannot occur -There are no recognizable EGC deflections; ventricles merely quiver (fibrillate) consuming a tremendous amount of oxygen -Patient is unresponsive with no pulse and little to no bp *-There is no cardiac output or pulse and therefore, no cerebral, myocardial, or systemic perfusion; this rhythm is rapidly fatal if not successfully ended within 3-5 minutes* -When Vfib begins, the patient becomes faint, immediately loses consciousness, and becomes pulseless and apneic; there is no blood pressure, and heart sounds are absent; respiratory and metabolic acidosis develop; seizures may occur; within minutes, the pupils become fixed and dilated and the skin becomes cold and mottled; death results without prompt intervention -The desired outcomes are to resolve VFib quickly and convert it to an organized rhythm, *therefore the priority is to defibrillate the patient immediately according to ACLS protocol; If a defibrillator is not readily available, CPR must be continued until the defibrillator arrives* -If VFib does not end after one defibrillator shock, the resuscitation team resumes high-quality CPR and provides airway management (intubation); the team also gives oxygen and drug therapy -Drug therapy includes: Epi, Vasopressin, Amiodarone, lidocaine and mag sulfate; alternating with defibrillation -If VFib is successfully converted to an organized rhythm, supportive care is continued *If we see VFib on monitor but walk into room and patient is awake, talking, etc., we check the monitor, leads, BP, etc.*

Ventricular tachycardia

VTach -Occurs with repetitive firing of an irritable ventricular etopic focus, usually at a rate of 140-180 bmp or more -The sinus node may continue to discharge independently, depolarizing the atria but not the ventricles, although P waves are seldom seen in sustained VTach -3 Categories: Stable, Unstable, Pulseless -May occur in patients with ischemic heart disease, MI, cardiomyopathy, hypokalemia, hypomagnesemia, valvular heart disease, heart failure, drug toxicity, hypotension, or ventricular aneurysm *In patients who go into cardiac arrest, VTach is commonly the initial rhythm before deterioration into VFib as the terminal rhythm!*

Diabetes Insipidus

Water metabolism problem caused by an ADH deficiency -ADH deficiency results in the excretion of large volumes of dilute urine; Without ADH, the kidneys do not reabsorb water, leading to *polyuria* and dehydration -Dehydration caused by the massive water loss causes thirst sensation which promotes increased fluid intake and aids in maintaining water balance; *if the thirst sensation is absent or if the patient is unable to obtain water, dehydration becomes more severe and can lead to death* *Signs and symptoms include: 4-30 L/day of dilute (pale yellow) urine with low specific gravity (less than 1.005) and low osmolarity (50-200 mOsm/kg); increased thirst; dehydration due to increased urine output; hemoconcentration; polydipsia due to increased thirst; hypotension; tachycardia; increased BUN; irritability, decreased cognition, hyperthermia, lethargy to coma, atatxia* *Complications include: hypovolemia, severe dehydration, hypernatremia, decreased cardiac output, unconsciousness, seizure, death* *Treatment includes; Diabinese for partial deficits; desmopressin/vasopressin for severe deficits- watch for fluid overload- weigh daily; administer/teach fluid intake equal to urine output- do not restrict fluids!*

Hepatitis E

Waterborne infection associated with epidemics in certain countries outside the US Many outbreaks occur after heavy rains and flooding Oral-fecal route; contaminated food and water Clinical course resembles Hep A Incubation period of 15-64 days Tend to be self-limiting and resolves on own= Not chronic like Hep C

Shock

Widespread abnormal cellular metabolism that occurs when oxygenation and tissue perfusion needs are not met to the level necessary to maintain cell function -A condition rather than a disease and represents a "whole body" response that occurs when too little oxygen is delivered to the tissues -All body organs are affected by shock and either work harder to adapt and compensate for reduced oxygenation or fail to function because of hypoxia -Any problem that impairs oxygen delivery to tissues and organs can start the syndrome of shock and lead to a life threatening emergency -Most often, shock is a result of cardiovascular problems and changes -When shock progresses, severe hypoxia can lead to cell loss, MODS, and death -Shock is classified by the functional impairment it causes into the categories of: Hypovolemic shock, Cardiogenic shock, Distributive shock (septic shock, neurogenic shock, and anaphylactic shock), and Obstructive shock -If left untreated, all shock leads to hypotension and then death