NURS 222 Study Guide Exam #1.pdf

NURS 222 Study Guide Exam #1 Chapter 28 Dysrhythmias- Hayat Generally: AKA- Arrhythmias Abnormal rhythms of the heart’s electrical system that can affect its ability to effectively pump oxygenated blood throughout the body. They are the resul...

NURS 222 Study Guide Exam #1 Chapter 28 Dysrhythmias- Hayat Generally: AKA- Arrhythmias Abnormal rhythms of the heart’s electrical system that can affect its ability to effectively pump oxygenated blood throughout the body. They are the result of disturbances in cardiac electrical impulse formation, conduction, or both. NORMAL SINUS RHYTHM (NSR) for Reference- ○ SA node ○ Normal resting heart rate from 60 to 100 bpm ○ Regular rhythm with consistent intervals between each heartbeat P wave should be upright in most leads, consistent in size and shape, and present before each QRS complex. ○ Normal PR interval: 0.12 to 0.20 seconds ○ QRS complex should last 0.04–0.44 seconds ○ ST segment follows the QRS complex and should be on the baseline. ○ QT interval varies based on heart rate but is generally up to 0.44 seconds. ○ T wave should be positive (upright) in most leads and less than 5 mm in height. SINUS TACHYCARDIA- PAGE 670, FIGURE 28. Rate: The heart rate is greater than 100 beats per minute, but usually doesn't exceed 180 beats per minute. Rhythm: The rhythm is regular, with P waves and QRS complexes marching out. P waves: P waves are present and normal and are upright in front of every QRS complex. At very fast rates, the P waves may merge with the T wave, creating a "camel hump" appearance. PR interval: The PR interval is normal and constant, between 0.12 and 0.20 seconds. QRS complex: The QRS complex is normal and less than 0.12 seconds after every P wave. Each QRS complex is preceded by a P wave. Signs and symptoms Usually asymptomatic Hypovolemia Dehydration Increased pulse rate Decreased urinary output Decreased blood pressure Dry skin and mucous membranes Anginal pain Palpitations Nursing intervention Assess vital signs at least every 4 hours and as needed. (similar to bradycardia in Monitor patient for cardiac dysrhythmias. terms of nursing Evaluate and document the patient’s response to dysrhythmias. interventions) Encourage the patient to notify the nurse when chest pain occurs. Assess chest pain (e.g., location, intensity, duration, radiation, precipitating and alleviating factors). Assess peripheral circulation (e.g., palpate for presence of  peripheral pulses, edema, capillary refill, color, temperature of extremity). Provide antidysrhythmic therapy according to unit policy (e.g., antidysrhythmic medication, cardioversion, defibrillation), as appropriate. Monitor and document patient’s response to antidysrhythmic medications or interventions. Monitor appropriate laboratory values (e.g., cardiac enzymes, electrolyte levels). Monitor the patient’s activity tolerance, and schedule exercise and rest periods to avoid fatigue. Observe for respiratory difficulty (e.g., shortness of breath, rapid breathing, labored respirations). Promote stress reduction. Offer pastoral/spiritual support to the patient and/or family (e.g., contact clergy), as appropriate. SINUS BRADYCARDIA(PAGE 670, FIGURE 28.8) Signs and symptoms Syncope (“blackouts” or fainting) Dizziness and weakness Confusion Hypotension Diaphoresis (excessive sweating) Shortness of breath Chest pain Nursing intervention Identify and treat the underlying cause if the patient is stable. Administer IV atropine if the cause is unclear, increase intravascular volume with IV fluids. Apply oxygen if oxygen saturation is below 94% or if the patient has shortness of breath. Discontinue any medications that may be causing bradycardia. Administer glucagon in cases of suspected beta-blocker overdose to increase heart rate and blood pressure.  Prepare for transcutaneous or transvenous pacing if the heart rate does not improve. Plan for permanent pacemaker implantation if normal sinus rhythm is not restored after addressing the underlying cause. ○ Artificial pacemaker An electrical device placed under skin near the clavicle Chapter 29 Cardiac Conditions 1. Heart Failure- Overview of Heart failure (HF) Clinical syndrome Characterized by s/s of ○ Fluid overload ○ Inadequate tissue perfusion Resulting from ○ Cardiac disorders that impair ventricular function Ventricles ability to fill or eject blood When the heart can't generate enough cardiac output (CO) to meet the body’s demands ○ Fluid overload/ decreased tissue perfusion result The term heart failure indicates a myocardial disease in which: ○ Systolic dysfunction—impaired contraction of the heart ○ Diastolic dysfunction— impaired filling of the heart ○ Cause pulmonary or systemic congestion Sometimes reversible Usually chronic/ progressive Managed w/ lifestyle changes and meds to prevent episodes of ○ Acute decompensated HF Increased symptoms Decreased CO2 Low perfusion Chronic Heart Failure ○ Most common > 75 years old ○ How to determine the type of HF: Echocardiogram to assess ejection fraction (EF)—reflects L ventricular function Normal EF: 55%-65% Means that the ventricle doesn’t completely empty between contractions ○ Two major types Systolic HF: Alteration in ventricular contraction Characterized by a weakened heart muscle Most common type  Reduced EF is hallmark Diastolic HF: Characterized by a stiff and noncompliant heart muscle Makes it difficult for ventricle to fill AKA heart failure w/ preserved EF— b/c EF is normal ○ Severity of HF is classified according to patients symptoms ○ New York Heart Association (NYHA) HF classifications: ○ Etiology (causes): ○ CAD ○ HTN: systemic or pulmonary Increases after load (resistance to ejection) Which increases cardiac workload Leads to hypertrophy— ventricles may dilate and fail ○ Cardiomyopathy Disease of the myocardium Dilated type: Causes necrosis/ fibrosis of myocytes Hypertrophic type: Leads to severe ventricular hypertrophy Poor diastolic filling (diastolic failure) HF due to cardiomyopathy is usually chronic/ progressive Sometimes can resolve if causative agent is removed ○ Valvular disorders Difficulty of blood to move forward Increases pressure and cardiac workload leading to HF ○ Renal dysfunction w/ volume overload More than 40% of patients w/ chronic HF have renal dysfunction ○ A-fib Can cause or result from HF  ○ Diabetes = increased risk ○ Atherosclerosis— primary cause Ischemia—causes deprivation of O2 and cell damage MI—causes heart muscle necrosis, cell death and loss of contractility Extent of infarction correlates w/ severity of HF Pathophysiology: ○ Significant myocardial dysfunction occurs before patient experiences s/s of HF such as SOB, edema or fatigue ○ As HF develops, the body activates neurohormonal compensatory mechanisms: Increased demand for cardiac output is required Ventricles dilate/ stretch to try and accommodate the need Ventricular hypertrophy Ventricle enlarges The muscle gets bigger overtime, making HF worse Increase in SNS stimulation w/ release of epinephrine and norepinephrine Vasoconstriction to skin, GI tract and kidneys Increased BP, HF and after load Kidneys response: Decrease in renal perfusion due to low CO2 and vasoconstriction causes the release of renin and stimulation of the RAAS Left-Sided Heart Failure ○ Formerly known as congestive heart failure ○ Fluid accumulates behind the L ventricle due to the inability of the L ventricle to pump blood out of the ventricle into the aorta and systemic circulation Due to increased blood volume and pressure, blood flow is decreased during L ventricle diastole Pulmonary venous blood volume and pressure increase in the lungs Forces fluid from the pulmonary capillaries into the pulmonary tissues and alveoli Causes pulmonary interstitial edema and impaired gas exchange ○ Clinical manifestations of congestion: Dyspnea/ SOB May complain of orthopnea— dyspnea when laying flat ○ Use pillows to prop up in bed or sleep sitting in chair Some patients have sudden attacks at of dyspnea at night (PND) ○ Fluid that accumulates in dependent extremities during the day may be reabsorbed in the circulating blood volume when the pt likes down The Impaired L ventricle can’t eject the increased blood volume Pressure in the pulmonary circulation increases, shifting fluid into he alveoli Fluid-filled alveoli cant exchange 02 and CO2 w/o sufficient 02 = dyspnea and difficulty sleeping Cough Cough assoc. w/ L ventricular failure is initially dry/ nonproductive  Usually complain of dry/ hack cough— mistaken for asthma or COPD May become moist overtime Large quantities of frothy sputum (pink/ tan [blood tinged])—indicated acute decompensated HF w/ pulmonary edema Pulmonary crackles Early phase— Usually bibasilar crackles that do not clear w/ cough As HF worsens— crackles through lung fields and decreased 02 Low 02 sat S3 or gallop may be auscultated— caused by abnormal ventricular filling The amount of blood ejected from the L ventricle is decreased, can lead to inadequate tissue perfusion Decrease in cardiac output causes low perfusion Decrease in stroke volume can stimulate the SNS to release catechalomines, which further impeded perfusion to many organs including kidneys Decreased renal perfusion: Oliguria ○ Reduced CO and catecholamines release decreased blood flow to the kidneys, and urine output drops ○ A decrease in renal perfusion pressure stimulates RAAS, causing increase in BP and intravascular volume ○ Nocturia— cardiac workload is decreased when pt is sleeping, improving renal perfusion (frequent urination @ night Decreased GI perfusion: Altered digestion Decreased brain perfusion: Dizziness Lightheadedness Confusion Restlessness Anxiety SNS stimulation also causes vasoconstriction Skin: Pallor Cool Decreased SV causes SNS to increase HR Tachycardia Palpations Weak pulses W/O adequate CO the body cant respond to energy demands W/O adequate CO the body can't respond to energy demands ○ Fatigue ○ Activity intolerance  Right-sided HF ○ Fluid accumulates being right ventricle ○ Right side of the heart cant eject blood effectively and cant accommodate all of the blood that normally returns to it from the venous circulation ○ Congestion in the peripheral tissues and viscera predominates ○ Increased venous pressure: JVD ○ Systemic clinical manifestations: Dependent edema (lower extremities) Usually feet and ankles—worse when pt stands or sits for a long period Can gradually progress up legs/ thighs to genitalia and lower trunk Sacral edema— common w/ bedrest Pitting edema— usually obvious after retention of at least 4.5 kg (10 lb) of fluid Hepatomegaly And tenderness in RUQ from venous engorgement May interfere w/ livers ability to function Ascites Evidenced by abdominal girth GI distress—increased pressure from on stomach/ intestines and Respiratory distress—increase pressure on diaphragm Weight gain- fluid retention Anorexia (loss of appetite)/ nausea/ abdominal pain From venous engorgement/ venous stasis within the abdominal organs Generalized weakness From reduced CO a. Signs and symptoms Manifestation are r/t congestion and poor perfusion or r/t what ventricle is affected most  In chronic HR, patients have s/s of both R and L ventricular failure b. Nursing teaching Call 911 if- ○ You have chest pain ○ Severe dizziness ○ Shortness of breath Call your provider if you ○ Gain 2-3 lbs within 24 hours or 5 pounds in a week ○ Have more trouble sleeping and cannot lie flat ○ Noticed increased swelling in your legs, feet, or ankles ○ More shortness of breath when you are active ○ Pain or swelling in your belly ○ Trouble sleeping ○ Dry, hacking cough ○ Keep a record of your daily weight ○ Take all your meds as instructed ○ Eat- a low-sodium diet ○ Stay active and enjoy life ○ Go to your follow-up appointments c. Nursing interventions Assessment ○ Focus- Effectiveness of therapy Patients self-management strategies S/S of increased HF - Emotional/ psychosocial response Interventions: ○ Promoting activity tolerance Daily walking walking regimen w/ increased duration over 6 weeks Alt. activities/ rest Avoid having two energy consuming activities on same day Small frequent meals Monitor patients response to activities ○ Managing fluid volume  Diuretics PO diuretics administered in am—so diuresis doesn’t interfere w/ sleep Discussing timing is esp. important for older adults who may have frequency/ incontinence Monitor fluid status Lung sounds Daily wt Adherence to low Na diet Positining Extra pillows Elevate HOB Recliner chair Support lower arms w/ pillows— eliminate fatigue caused by the pull of weight on shoulders Positioning to avoid pressure/ frequent changes Control anxiety Minimizing powerlessness Assist with effective health management Monitoring/ managing potential complications: Acute decompensated HF Pulmonary edema Kidney injury Dysrhythmias Many problems assoc/ w HF are r/t diuretic use: Many problems assoc/ w HF are r/t diuretic use: ○ Hypokalemia— from excessive/ repeated diuresis; can lead to dig toxicity if taking digoxin Ventricular dysrhythmias Hypotension Muscle weakness Generalized weakness ○ Low mag— at risk for dysrhythmias ○ Hyperkalemia— esp w/ use of ACE inhibitors, ARBs, spironactone Profound bradycardia/dysrhythmias ○ Hyponatremia-from prolonged diuretic use ○ Disorientation ○ Weakness ○ Muscle cramps ○ Anorexia Volume depletion from excessive fluid loss ○ Dehydration ○ Hypotension (ACE inhibitors/ beta-blockers can contribute)  Other problems associated with diuretics: ○ Increased Creatinine- renal dysfunction ○ Hyperuricemia- excessive uric acid leading to gout d. Priority of care Increasing gas exchange Increasing perfusion Preventing or managing pulmonary edema Monitor side effects of meds being given 2. Mitral valve prolapse- Hayat a. Signs and symptoms Valvular leaflets enlarge and prolapse into the left atrium during systole. In another words, the mitral valve won’t completely close during systole, thus blood regurgitates from the left ventricle to the left atrium. Etiology varies; has a family tendency but it is common in females Most people are asymptomatic Some may report fatigue chest pain, shortness of breath, lightheadedness, dizziness, syncope (fainting), palpitations, exercise intolerance, anxiety May have mid systolic click and late systolic murmur at apex b. Nursing intervention Dietary restrictions (epinephrine, alcohol, caffeine, ephedrine) Smoking cessation Mitral valve/replacement Minimize infection risk b/c these patients can easily develop endocarditis (inflamed endocardium)  No piercing/tattoos plus practice safe oral hygiene 3. Chronic obstructive pulmonary disease a. Signs and symptoms: - Dyspnea, productive cough, wheezing, hypoxia, cyanosis, use of accessory muscles, clubbing of the fingers, barrel-shaped chest, b. Laboratory as s/s and outcome evaluation c. Pathophysiology: lower airway disorders that interfere w/airflow and gas exchange. These disorders include Emphysema & Bronchitis Emphysema Bronchitis - Overdistention of alveoli w/ trapped air - Hypersecretion of mucus in the large which creates obstruction to expiratory and small airways, hypoxia, cyanosis. airflow, loss of elastic recoil of the - Difficulty taking air IN alveoli, & high residual volume of CO2. - Cough, clubbing of the fingers - Difficulty getting air OUT - BLUE BLOATER b/c cyanosis - Chronic hypercapnia, prolonged - Inflammation causes permanent exhalation, barrel-shaped chest damage and the edema that results - PINK PUFFER b/c they remain well from Rt ventricular failure oxygenated and use pursed-lip breathing d. Risk factors e. Cor pulmonale (complication): - Complications of severe COPD are in areas of poor ventilation, hypoxia stimulates pulmonary arterial vasoconstriction AKA pulmonary HTN which causes resistance in the main pulmonary artery in turn increasing the resistance against the right ventricle. This lead to Rt ventricle hypertrophy and eventually Rt ventricular heart failure. - S/Sx: JVD, ascites, hepatomegaly, splenomegaly, edema 4. Chest tube management a. Priority of care ` b. Drainage system and nursing responsibility - Closed drainage system - Bubbling of water in the water-seal indicates air drainage from the patient which is seen when pt exhales, coughs, or sneezes. When air in the pleural space has been removed bubbling stops however, a blocked or kinked tube can also cause the bubbling to stop. Excessive bubbling can indicate air leak. - Tidaling: rise of 2-4 inches in the water-seal chamber during inhalation that falls during exhalation. - Nursing Care: - Assess for difficulty breathing. - Assess breathing effectiveness by pulse oximetry. - Listen to breath sounds for each lung. - Check alignment of trachea.  - Check tube insertion site for condition of the skin. Palpate area for puffiness or crackling that may indicate subcutaneous emphysema. - Observe site for signs of infection - Assess for pain. - Assist patient to deep breathe, cough, perform maximal sustained inhalations, and use incentive spirometry. - Reposition the patient who reports a “burning” pain in the chest. - Keep drainage system lower than the level of pt chest - Avoid kinks or loops Chapter 17 Human Immunodeficiency Virus - Progressive depletion of CD4 T cells which are important for cell-mediated and antibody-mediated immune mechanisms the two strongest ways to fight infection. It is a retrovirus meaning is contains RNA as its genetic material and comes with reverse transcriptase which can convert its RNA into DNA. HIV enters CD4 Tcells and turns the cells into a virus factory making these cells inactive. - Everyone with AIDs has HIV however not everyone with HIV has AIDs. - Has 3 stages: - Acute: - Fever, headache, fatigue, pharyngitis, GI symptoms, lymphadenopathy, arthralgias, myalgia, sore throat, rash, night sweats. - Within 28 days - Chronic: - Latent stage - Asymptomatic, if untreated increased levels of viremia and decreased levels of CD4 cells occur - 6 months - 10 years - AIDS: - CD4