Nursing Assessment for Osteoarthritis

Osteoarthritis

Hypertrophic osteoarthritis; Osteoarthrosis; Degenerative joint disease; DJD; OA; Arthritis - osteoarthritis

• Osteoarthritis

Nursing Assessment for Osteoarthritis

1. Activity / Rest
   • Joint pain due to movement, tenderness worsened by stress on the joints, stiffness in the morning, usually occurs bilaterally and symmetrically functional limitations that affect lifestyle, leisure, work, fatigue, malaise.
   • Limitation of movement, muscle atrophy, skin: contractor / abnormalities in the joints and muscles.
2. Cardiovascular
   • Raynaud's phenomenon of the hand (eg litermiten pale, cyanosis and redness on the fingers before the color returned to normal.
3. Ego Integrity
   • Stress factors of acute / chronic (eg, financial jobs, disability, relationship factors.
   • Hopelessness and helplessness (inability situation).
   • Threats to the self-concept, body image, personal identity, for example dependence on others.
4. Food / Fluids
   • The inability to produce or consume food or liquids adequately nausea, anorexia.
   • Difficulty chewing, weight loss, dryness of mucous membranes.
5. Hygiene
   • The difficulties to implement self-care activities, dependence on others.
6. Neurosensory
   • Tingling in hands and feet, swollen joints
7. Pain / comfort
   • The acute phase of pain (probably not accompanied by soft tissue swelling in the joints. chronic pain and stiffness (especially in the morning).
8. Security
   • Skin shiny, taut, nodules sub mitaneus
   • Skin lesions, foot ulcers
   • The difficulty in handling the task / household maintenance
   • Mild fever settled
   • Dryness in the eyes and mucous membranes
9. Social Interaction
   • Damage interaction with family or others, the changing role: isolation.
10. Counseling / Learning
    • Family history of rheumatic
    • The use of health foods, vitamins, cure disease without testing
    • History pericarditis, valve lesion edge. Pulmonary fibrosis, pleuritis.

death Anxiety

Taxonomy II: Coping/Stress Tolerance—Class 2 Coping Response (00147)
[Diagnostic Division: Ego Integrity]
Submitted 1998

Definition: Apprehension, worry, or fear related to death or dying

Related Factors
To be developed

Defining Characteristics
SUBJECTIVE

Fear of: developing a terminal illness; the process of dying; loss of physical and/or mental abilities when dying; premature death because it prevents the accomplishment of important life goals; leaving family alone after death; delayed demise

Negative death images or unpleasant thoughts about any event related to death or dying; anticipated pain related to dying

Powerlessness over issues related to dying; total loss of control over any aspect of one’s own death

Worrying about: the impact of one’s own death on SOs; being the cause of other’s grief and suffering

Concerns of overworking the caregiver as terminal illness incapacitates self; about meeting one’s creator or feeling doubtful about the existence of God or higher being

Denial of one’s own mortality or impending death
OBJECTIVE
Deep sadness
(Refer to ND anticipatory Grieving.)


Desired Outcomes/Evaluation
Criteria—Client Will:
• Identify and express feelings (e.g., sadness, guilt, fear) freely/effectively.
• Look toward/plan for the future one day at a time.
• Formulate a plan dealing with individual concerns and eventualities of dying.

Actions/Interventions
NURSING PRIORITY NO.1. To assess causative/contributing factors:
• Determine how client sees self in usual lifestyle role functioning and perception and meaning of anticipated loss to him or her and SO(s).
• Ascertain current knowledge of situation to identify misconceptions, lack of information, other pertinent issues.
• Determine client’s role in family constellation. Observe patterns of communication in family and response of family/ SO to client’s situation and concerns. In addition to identifying areas of need/concern, also reveals strengths useful in addressing the concerns.
• Assess impact of client reports of subjective experiences and past experience with death (or exposure to death); for example, witnessed violent death or as a child viewed body in casket, and so on.
• Identify cultural factors/expectations and impact on current situation/feelings.
• Note physical/mental condition, complexity of therapeutic regimen.
• Determine ability to manage own self-care, end-of-life and other affairs, awareness/use of available resources.
• Observe behavior indicative of the level of anxiety present (mild to panic)  as it affects client’s/SO’s ability to process information/participate in activities.
• Identify coping skills currently used and how effective they are. Be aware of defense mechanisms being used by the client.
• Note use of drugs (including alcohol), presence of insomnia, excessive sleeping, avoidance of interactions with others.
• Note client’s religious/spiritual orientation, involvement in religious/church activities, presence of conflicts regarding spiritual beliefs.
• Listen to client/SO reports/expressions of anger/concern, alienation from God, belief that impending death is a punishment for wrongdoing, and so on.
• Determine sense of futility, feelings of hopelessness, helplessness, lack of motivation to help self.May indicate presence of depression and need for intervention.
• Active-listen comments regarding sense of isolation.
• Listen for expressions of inability to find meaning in life or suicidal ideation.  NURSING PRIORITY NO.2. To assist client to deal with situation:
• Provide open and trusting relationship.
• Use therapeutic communication skills of Active-listening, silence, acknowledgment. Respect client desire/request not to talk. Provide hope within parameters of the individual situation.
• Encourage expressions of feelings (anger, fear, sadness, etc.). Acknowledge anxiety/fear. Do not deny or reassure client that everything will be all right. Be honest when answering questions/providing information. Enhances trust and therapeutic relationship.
• Provide information about normalcy of feelings and individual grief reaction.
• Make time for nonjudgmental discussion of philosophic issues/questions about spiritual impact of illness/situation.
• Review life experiences of loss and use of coping skills, noting client strengths and successes.
• Provide calm, peaceful setting and privacy as appropriate. Promotes relaxation and ability to deal with situation.
• Assist client to engage in spiritual growth activities, experience prayer/meditation and forgiveness to heal past hurts. Provide information that anger with God is a normal part of the grieving process. Reduces feelings of guilt/conflict, allowing client to move forward toward resolution.
• Refer to therapists, spiritual advisors, counselors to facilitate grief work.
• Refer to community agencies/resources to assist client/SO for planning for eventualities (legal issues, funeral plans, etc.).
NURSING PRIORITY NO.3. To promote independence:
• Support client’s efforts to develop realistic steps to put plans into action.
• Direct client’s thoughts beyond present state to enjoyment of each day and the future when appropriate.
• Provide opportunities for client to make simple decisions. Enhances sense of control.
• Develop individual plan using client’s locus of control  to assist client/family through the process.
• Treat expressed decisions and desires with respect and convey to others as appropriate.
• Assist with completion of Advance Directives and cardiopulmonary resuscitation (CPR) instructions.


Documentation Focus
ASSESSMENT/REASSESSMENT
• Assessment findings, including client’s fears and signs/symptoms being exhibited.
• Responses/actions of family/SO(s).
• Availability/use of resources.
PLANNING
• Plan of care and who is involved in planning.
IMPLEMENTATION/EVALUATION
• Client’s response to interventions/teaching and actions performed.
• Attainment/progress toward desired outcome(s).
• Modifications to plan of care.
DISCHARGE PLANNING
• Identified needs and who is responsible for actions to be taken.
• Specific referrals made.

Nursing Care Plan Lung Cancer Postoperative Care

Lung cancer picture

Lung cancers can arise in any part of the lung, but 90%-95% of cancers of the lung are thought to arise from the epithelial cells, the cells lining the larger and smaller airways (bronchi and bronchioles); for this reason, lung cancers are sometimes called bronchogenic cancers or bronchogenic carcinomas. (Carcinoma is another term for cancer.) Cancers also can arise from the pleura (called mesotheliomas) or rarely from supporting tissues within the lungs, for example, the blood vessels.
source : http://www.medicinenet.com
LUNG CANCER: POSTOPERATIVE CARE
I. Pathophysiology
a. Usually develops within the wall or epithelium of the bronchial tree
b. Prolonged exposure to cancer-promoting agents causes damage to ciliated cells and mucus-producing cells, leading
to genetic mutations and development of dysplastic cells.
II. Classification (Memorial Sloan-Kettering Cancer Center, 2008; National Cancer Institute, 2008)
a. Small cell lung cancers (SCLCs), or oat cell lung cancer
i. Represent about 15% to 25% of lung cancer cases (Elias & Baldini, 2008)
ii. Occur almost exclusively in smokers
iii. Aggressive and fast growing with surgery seldom a treatment option
b. Non–small cell lung cancers (NSCLCs)
i. Most common type of lung cancer (75% to 85%, Elias & Baldini, 2008)
ii. Include adenocarcinoma, squamous cell, and large cell carcinomas
iii. Frequently associated with metastases, but are generally slow growing
III. Staging (National Cancer Institute, 2008)
a. Stage 0—cancer cells only found in the innermost lining of the lung
b. Stage IA—tumor has grown through the innermost lining of the lung into deeper lung tissue, but does not invade the
bronchus; no cancer cells found in nearby lymph nodes
c. Stage IB—tumor is larger, may be more than 3 cm across; may have grown into the main bronchus; may have grown
into the pleura, but no cancer cells found in nearby lymph nodes
d. Stage IIB—tumor has invaded the chest wall, diaphragm, pleura, main bronchus, or tissue that surrounds the heart;
cancer cells found in nearby lymph nodes
e. Stage IIIA—tumor may be any size; cancer cells found in the lymph nodes near the lungs and bronchi and between
the lungs on the same side of the chest as the tumor
f. Stage IIIB—tumor may be any size; cancer cells found on the opposite side of the chest from the tumor, with possible
invasion into nearby organs
g. Stage IV—malignant growths may be found in more than one lobe or may have metastasized to other organs
IV. Etiology (American Cancer Society, 2008)
a. Risk factors include cigarette smoking or being exposed to secondhand smoke; radon, asbestos, other occupational
exposures, including radioactive ores such as uranium, inhaled chemicals or minerals, such as nickel compounds, silica, coal dust, and cromates, or diesel exhaust; high levels of arsenic in drinking water; and family history of lung cancer.
b. Chronic obstructive pulmonary disease (COPD) and pulmonary fibrosis may increase susceptibility.
V. Statistics
a. Morbidity: Second most commonly diagnosed cancer accounting for 13% of all cases (American Association
for Cancer Research, 2005) with new cases of lung and bronchus cancer estimated at 172,570 for 2005 (Jemal et al, 2005).
b. Mortality: Number one cause of death in cancer patients; in 2004, death rates for men and women were 89,575 and 68,431, respectively; results in more deaths than breast cancer, prostate cancer, and colon cancer combined (U.S. Cancer Statistics Worling Group, 2007).
c. Cost: $9.6 billion was spent for treatment in 2004.
VI. Treatment Options
a. Depends upon staging—generally the lower the stage, the more favorable the prognosis
i. Surgery is primary treatment for NSCLC stage I and stage II tumors.
ii. Selected stage III carcinomas may be operable if the tumor is resectable.
b. Surgical procedures for operable tumors of the lung include:
i. Pneumonectomy—performed for lesions originating in the main stem bronchus or lobar bronchus
ii. Lobectomy—preferred for peripheral carcinoma localized in a lobe
iii.Wedge or segmental resection—performed for lesions that are small and well contained within one segment
iv. Endoscopic laser resection—may be done on peripheral tumors to reduce the necessity of cutting through ribs
v. Photodynamic therapy—reduces symptoms such as bleeding or may be used to treat very small tumors


Care Setting
Client is treated in inpatient surgical and possibly subacute units.
Nursing Priorities
1. Maintain or improve respiratory function.
2. Control or alleviate pain.
3. Support efforts to cope with diagnosis and situation.
4. Provide information about disease process, prognosis, and therapeutic regimen.
Discharge Goals
1. Oxygenation and ventilation adequate to meet individual activity needs.
2. Pain controlled.
3. Anxiety and fear decreased to manageable level.
4. Free of preventable complications.
5. Disease process, prognosis, and planned therapies understood.
6. Plan in place to meet needs after discharge.
NURSING DIAGNOSIS: impaired Gas Exchange
May be related to
Removal of lung tissue
Altered oxygen supply—hypoventilation
Decreased oxygen-carrying capacity of blood—blood loss
Possibly evidenced by
Dyspnea
Restlessness
Changes in mentation
Hypoxemia and hypercapnia
Cyanosis
Desired Outcomes/Evaluation Criteria—Client Will
Respiratory Status: Gas Exchange
Demonstrate improved ventilation and adequate oxygenation of tissues by arterial blood gases (ABGs) within client’s normal range.
Be free of symptoms of respiratory distress.
ACTIONS/INTERVENTIONS
Respiratory Management
Independent
Note respiratory rate, depth, and ease of respirations. Observe for use of accessory muscles, pursed-lip breathing, or changes in skin or mucous membrane color, such as pallor and cyanosis.
Auscultate lungs for air movement and abnormal breath sounds.
Investigate restlessness and changes in mentation and level of consciousness.
Assess client response to activity. Encourage rest periods, limiting activities to client tolerance.
Note development of fever.
Airway Management
Maintain patent airway by positioning, suctioning, and use of airway adjuncts.
Reposition frequently, placing client in sitting and supine to side positions.
Avoid positioning client with a pneumonectomy on the operative side; instead, favor the “good lung down” position.
Encourage and assist with deep-breathing exercises and pursed-lip breathing, as appropriate.
Tube Care: Chest
Maintain patency of chest drainage system following lobectomy and segmental wedge resection procedures.
Note changes in amount or type of chest tube drainage.
Observe for presence of bubbling in water-seal chamber.
Airway Management
Collaborative
Administer supplemental oxygen via nasal cannula, partial rebreathing mask, or high-humidity face mask, as indicated.
Assist with and encourage use of incentive spirometer.
Monitor and graph ABGs and pulse oximetry readings. Note hemoglobin (Hgb) levels.
RATIONALE
Respirations may be increased as a result of pain or as an initial compensatory mechanism to accommodate for loss of lung tissue. However, increased work of breathing and cyanosis may indicate increasing oxygen consumption and energy expenditures or reduced respiratory reserve, for example, in an elderly client or extensive COPD.
Consolidation and lack of air movement on operative side are normal in the client who has had a pneumonectomy; however, a client who has had a lobectomy should demonstrate normal airflow in remaining lobes.
May indicate increased hypoxia or complications such as mediastinal shift in a client who has had a pneumonectomy when accompanied by tachypnea, tachycardia, and tracheal deviation.
Increased oxygen consumption and demand and stress of surgery may result in increased dyspnea and changes in vital signs with activity; however, early mobilization is desired to help prevent pulmonary complications and to obtain and maintain respiratory and circulatory efficiency.
Adequate rest balanced with activity can prevent respiratory compromise.
Fever within the first 24 hours after surgery is frequently due to atelectasis. Temperature elevation within postoperative day 5 to 10 usually indicates an infection, such as wound or systemic.
Airway obstruction impedes ventilation, impairing gas exchange. (Refer to ND: ineffective Airway Clearance.)
Maximizes lung expansion and drainage of secretions.
Research shows that positioning clients following lung surgery with their “good lung down” maximizes oxygenation by using gravity to enhance blood flow to the healthy lung, thus creating the best possible match between ventilation and perfusion.
Promotes maximal ventilation and oxygenation and reduces or prevents atelectasis.
Drains fluid from pleural cavity to promote reexpansion of remaining lung segments.
Bloody drainage should decrease in amount and change to a more serous composition as recovery progresses.
A sudden increase in amount of bloody drainage or return to frank bleeding suggests thoracic bleeding or a hemothorax; sudden cessation suggests blockage of tube, requiring further evaluation and intervention.
Air leaks appearing immediately postoperatively are not uncommon, especially following lobectomy or segmental resection; however, this should diminish as healing progresses. Prolonged or new leaks require evaluation to identify problems in client versus a problem in the drainage system.
Maximizes available oxygen, especially while ventilation is reduced because of anesthetic, depression, or pain, and during period of compensatory physiological shift of circulation to remaining functional alveolar units.
Prevents or reduces atelectasis and promotes reexpansion of small airways.
Decreasing PaO2 or increasing PaCO2 may indicate need for ventilatory support. Significant blood loss results in decreased oxygen-carrying capacity, reducing PaO2.

Nursing Care Plan for Congestive Heart Failure - CHF

What is congestive heart failure?

Congestive heart failure (CHF) is a condition in which the heart's function as a pump is inadequate to deliver oxygen rich blood to the body. Congestive heart failure can be caused by:

1. diseases that weaken the heart muscle,
2. diseases that cause stiffening of the heart muscles, or
3. diseases that increase oxygen demand by the body tissue beyond the capability of the heart to deliver adequate oxygen-rich blood.

The heart has two atria (right atrium and left atrium) that make up the upper chambers of the heart, and two ventricles (left ventricle and right ventricle) that make up the lower chambers of the heart. The ventricles are muscular chambers that pump blood when the muscles contract. The contraction of the ventricle muscles is called systole.
Many diseases can impair the pumping action of the ventricles. For example, the muscles of the ventricles can be weakened by heart attacks or infections (myocarditis). The diminished pumping ability of the ventricles due to muscle weakening is called systolic dysfunction. After each ventricular contraction (systole) the ventricle muscles need to relax to allow blood from the atria to fill the ventricles. This relaxation of the ventricles is called diastole.


Congestive heart failure can affect many organs of the body. For example:

• The weakened heart muscles may not be able to supply enough blood to the kidneys, which then begin to lose their normal ability to excrete salt (sodium) and water. This diminished kidney function can cause the body to retain more fluid.
• The lungs may become congested with fluid (pulmonary edema) and the person's ability to exercise is decreased.
• Fluid may likewise accumulate in the liver, thereby impairing its ability to rid the body of toxins and produce essential proteins.
• The intestines may become less efficient in absorbing nutrients and medicines.
• Fluid also may accumulate in the extremities, resulting in edema (swelling) of the ankles and feet.

Eventually, untreated, worsening congestive heart failure will affect virtually every organ in the body.
Heart failure also affects the kidneys' ability to dispose of sodium and water. The retained water increases the edema.

Congestive Heart Failure Symptoms and Signs
The symptoms of congestive heart failure vary among individuals according to the particular organ systems involved and depending on the degree to which the rest of the body has "compensated" for the heart muscle weakness.
The early symptoms are often shortness of breath, cough, or a feeling of not being able to get a deep breath.
In addition, the three major symptoms of congestive heart failure are :

1. exercise intolerance (a person may be unable to tolerate exercise or even mild physical exertion that he or she may have been able to do in the past);
2. shortness of breath (you may have difficulty breathing (dyspnea), especially when active, or even at rest); and
3. fluid retention and swelling (edema in the legs, feet, and ankles).

Nursing Diagnosis

1. Decreased cardiac out put related to structural defect, myocardial dysfunction.
Ineffective breathing pattern related to pulmonary congestion.
2. Anxiety related to threat to or change in health status resulting in inability to manage feelings of uncertainty and apprehension regarding the life-style changes.
3. Disturbance of sleep pattern related to illness resulting in interrupted sleep caused by nocturnal dyspnea.

Nursing Intervention

• Monitor vital signs every two to four hours including apical pulse, peripheral pulses, capillary refill, CVP and PAP if appropriate. Indicates change in cardiac status and potential for arrhythmias, compromised systemic venous flow.
• Monitor for heart sounds and breath sounds. Indications of recuced cardiac output caused by mechanical failure, pulmonary edema.
• Monitor electrolyte level of sodium increases and potassium decreases. Diuretic therapy may induce hypokalemia; decreased glomerular filtration rate (GFR) may cause hypernatremia; arrhythmias may be induced by potassium imbalances.
• Administer diuretic (hydrochlorothiazide, furosemide) while monitoring for electrolyte imbalances. Acts on distal tubule to increase water and potassium excretion or loop of Henle to promote excretion of sodium and chloride.
• Administer bronchodilator (theophylline). Dilates airways to facilitate breathing if dyspneic.
• Administer inotropic agents (digoxin, dopamine) while monitoring hemodynamic status. Increases cardiac output by increasing cardiac contractility.
• Administer oxygen therapy by cannula. Provides oxygen if hypoxic from decreased cardiac output or with ventilation perfusion imbalance from fluid in alveoli.
• Provide quite environment limiting stimuli. Stimuli and stress stimulate catecholamines and cardiac workload.
• Provide small meals six times per day. Reduces pressure on diaphragm and enhances chest expansion.
• Provide bed rest with head of bed elevated 30 to 60 degrees. Promotes lung expansion and decreases venous return.
• Perform deep breathing exercises, incentive spirometry ever two hours. Improves breathing and oxygen intake.

Label: Nursing Care Plan, Nursing Care Plan for Congestive Heart Failure - CHF

Nursing Care Plan for Bronchiectasis

What Is Bronchiectasis?

Bronchiectasis (brong-ke-EK-ta-sis) is a condition in which damage to the airways causes them to widen and become flabby and scarred. The airways are tubes that carry air in and out of your lungs.
Bronchiectasis usually is the result of an infection or other condition that injures the walls of your airways or prevents the airways from clearing mucus. Mucus is a slimy substance that the airways produce to help remove inhaled dust, bacteria, and other small particles.
In bronchiectasis, your airways slowly lose their ability to clear out mucus. When mucus can't be cleared, it builds up and creates an environment in which bacteria can grow. This leads to repeated, serious lung infections.
Each infection causes more damage to your airways. Over time, the airways lose their ability to move air in and out. This can prevent enough oxygen from reaching your vital organs.
Bronchiectasis can lead to serious health problems, such as respiratory failure, atelectasis (at-eh-LEK-tah-sis), and heart failure.

Nursing Care Plan for Bronchiectasis

Bronchiectasis
Bronchiectasis is destruction and widening of the large airways.

• If the condition is present at birth, it is called congenital bronchiectasis.
• If it develops later in life, it is called acquired bronchiectasis.

Causes
Bronchiectasis is often caused by recurrent inflammation or infection of the airways. It most often begins in childhood as a complication from infection or inhaling a foreign object.
Cystic fibrosis causes about half of all bronchiectasis in the United States. Recurrent, severe lung infections (pneumonia, tuberculosis, fungal infections), abnormal lung defenses, and obstruction of the airways by a foreign body or tumor are some of the risk factors.
The condition can also be caused by routinely breathing in food particles while eating.
Symptoms

Symptoms often develop gradually, and may occur months or years after the event that causes the bronchiectasis.
They may include :

• Bluish skin color
• Breath odor
• Chronic cough with large amounts of foul-smelling sputum
• Clubbing of fingers
• Coughing up blood
• Cough that gets worse when lying on one side
• Fatigue
• Paleness
• Shortness of breath that gets worse with exercise
• Weight loss
• Wheezing

www.nlm.nih.gov
Assessment

1. History or presence of supporting factors
   • Smoking
   • Living or working in areas with severe air pollution
   • History of allergies in the family
   • There is a history of acid in childhood.
2. History or the presence of trigger factors such exacerbations :
   • Allergen (pollen, dust, skin, pollen or fungal)
   • Emotional Sress
   • Excessive physical activity
   • Air pollution
   • Respiratory tract infections
   • The failure of the recommended treatment program
3. Physical examination by focusing on the respiratory system include :
   • Assess the frequency and respiratory rhythm
   • Inpeksi color of skin and mucosal color menbran
   • Auscultation of breath sounds
   • Make sure that when patients use accessory muscles when breathing :
     • Lifting the shoulders during breathing
     • retraction abdominal muscles during breathing
     • Respiratory nostril
   • Assess if the symmetrical or asymmetrical chest expansion
   • Assess if the chest pain on breathing
   • Assess cough (whether productive or nonproductive). When you specify the color of sputum productive.
   • Determine if the patient has dispneu or orthopneu
   • Assess the level of consciousness.

Nursing Diagnosis and Intervention

1. Ineffective airway clearance related to increased production of viscous secretions or secretion.Goal :
   Keep the airway patent with breath sounds clean / clear. Result Criteria :
   Showed the behavior to improve airway clearance (effective cough, and issued a secret.
   Action Plan :
   
   • Monitor the frequency of respiration. Note the ratio of inspiration and expiration.
   • Auscultation of breath sounds and record breath sounds.
   • Assess the patient to a comfortable position, height headboard and sat on the back of the bed.
   • Help the abdominal breathing exercise or lip.
   • Observations karakteriktik cough and Auxiliary measures for effectiveness cough efforts.
   • Depth of fluid intake till 3000ml/day appropriate cardiac tolerance and provide a warm and fluid intake between meals in lieu.
   • Give the drug as indicated.
2. Changes in nutrition less than body requirements related to nausea, vomiting, sputum production, dispneu.Goal :
   Improvement in nutritional status and body weight patients Result Criteria :
   Patients did not experience further weight loss or maintain weight.
   Plan of action :
   
   • Monitor input and output every 8 hours, the amount of food consumed and body weight are weighed each week.
   • Create a fun atmosphere, an environment free of odor during mealtimes.
   • Refer patient to a dietitian to monitor food plan that will be consumed.
   • Encourage clients to drink at least 3 liters of fluid per day, if not get an IV.

Label: Nursing Care Plan, Nursing Care Plan for Bronchiectasis

Nursing Care Plan for Myocardial Infarction

Nursing Care Plan for Myocardial Infarction

Myocardial infarction (MI)
Myocardial infarction (MI) or acute myocardial infarction (AMI), commonly known as a heart attack, is the interruption of blood supply to a part of the heart, causing heart cells to die. This is most commonly due to occlusion (blockage) of a coronary artery following the rupture of a vulnerable atherosclerotic plaque, which is an unstable collection of lipids (fatty acids) and white blood cells (especially macrophages) in the wall of an artery. The resulting ischemia (restriction in blood supply) and oxygen shortage, if left untreated for a sufficient period of time, can cause damage or death (infarction) of heart muscle tissue (myocardium).
The electrocardiographic result of an acute myocardial infarction is seen below. (See Etiology.)
The electrocardiogram shows lateral ST-segment elevation that is consistent with a lateral wall acute myocardial infarction.


Myocardial infarction is considered part of a spectrum referred to as acute coronary syndrome (ACS). The ACS continuum representing ongoing myocardial ischemia or injury consists of unstable angina, non–ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI). Patients with ischemic discomfort may or may not have ST-segment or T-wave changes denoted on the electrocardiogram (ECG). ST elevations seen on the ECG reflect active and ongoing transmural myocardial injury. Without immediate reperfusion therapy, most persons with STEMI develop Q waves, reflecting a dead zone of myocardium that has undergone irreversible damage and death. Those without ST elevations are diagnosed either with unstable angina or NSTEMI?differentiated by the presence of cardiac enzymes. Both these conditions may or may not have changes on the surface ECG, including ST-segment depression or T-wave morphological changes.
Myocardial infarction may lead to impairment of systolic or diastolic function and to increased predisposition to arrhythmias and other long-term complications.
Assessment
Set basic management to obtain information about the current status of the patient so that all the deviations that occur can be known.

1. History or presence of risk factors :
   • Arterial disease.
   • Previous heart attack.
   • Family history of heart disease / heart attack positive.
   • High serum cholesterol (above 200 mg / L).
   • Smoker
   • A diet high in salt and high in fat.
   • Obesity. (Ideal body weight = (height -100 ± 10%))
   • Women after menopause because estrogen therapy.
2. Physical examination: based on cardiovascular assessment may indicate :
   Chest pain decreases with rest or administration of nitrate (the most important findings) are often also accompanied by : 
   • Feeling faint and / or death threats
   • Diaphoresis.
   • Nausea and vomiting sometimes.
   • Dispneu.
   • Syndrome in various stages of shock (pale, cold, moist or wet skin, lower blood pressure, rapid pulse, decreased peripheral pulse and heart sounds).
   • Fever (within 24-48 hours).
3. Review of chest pain in relation to :
   • Stimulating factor.
   • Quality.
   • Location.
   • Weight.

Nursing Diagnosis
Painful related to tissue ischaemia secondary to arterial blockage coroner. Possible evidenced by: chest pain with or without spread, face grimacing, restlessness, delirium changes in pulse and blood pressure.
Nursing Intervention
Objectives : Pain decreased after treatment action during ...
Criteria : Chest pain scale decreased for example from 3 to 2, or from 2 to 1, facial expression relaxed / calm, not tense, not restless pulse 60-100 x / minute, blood pressure 120/80 mmHg
Intervention :

• Observation of the characteristics, location, time, and travel is chest pain.
• Instruct the client to stop activity and rest during an attack.
• Help the client to do relaxation techniques, eg deep breathing, distraction behavior, visualization, or the guidance of imagination.
• Keep Olsigenasi with bikanul example (2-4 L / min)
• Monitor vital signs (pulse and blood pressure) every two hours.
• Collaboration with the health team in providing analgesic.

Label: Nursing Care Plan, Nursing Care Plan for Myocardial Infarction

Anxiety [specify level: mild, moderate, severe, panic] - Definition, Related Factors and Characteristics

Taxonomy II: Coping/Stress Tolerance—Class 2 Coping Responses (00146)
[Diagnostic Division: Ego Integrity]
Submitted 1973; Revised 1982, and 1998 (by small group work 1996)
Definition: Vague uneasy feeling of discomfort or dread accompanied by an autonomic response (the source often nonspecific or unknown to the individual); a feeling of apprehension caused by anticipation of danger. It is an altering signal that warns of impending danger and enables the individual to take measures to deal with threat.
Related Factors
Unconscious conflict about essential [beliefs]/goals and values of life
Situational/maturational crises
Stress
Familial association/heredity
Interpersonal transmission/contagion
Threat to self-concept [perceived or actual]; [unconscious conflict]
Threat of death [perceived or actual]
Threat to or change in health status [progressive/debilitating disease, terminal illness], interaction patterns, role function/ status, environment [safety], economic status
Unmet needs
Exposure to toxins
Substance abuse
[Positive or negative self-talk]
[Physiological factors, such as hyperthyroidism, pheochromocytoma, drug therapy, including steroids]


Defining Characteristics
SUBJECTIVE
Behavioral
Expressed concerns due to change in life events
Affective
Regretful; scared; rattled; distressed; apprehension; uncertainty; fearful; feeling inadequate; anxious; jittery; [sense of impending doom]; [hopelessness]
Cognitive
Fear of unspecific consequences; awareness of physiological symptoms
Physiological
Shakiness; worried; regretful; dry mouth (s); tingling in extremities (p); heart pounding (s); nausea (p); abdominal pain (p); diarrhea (p); urinary hesitancy (p); urinary frequency (p); faintness (p); weakness (s); decreased pulse (p); respiratory difficulties (s); fatigue (p); sleep disturbance (p); [chest, back, neck pain]
OBJECTIVE
Behavioral
Poor eye contact; glancing about; scanning and vigilance; extraneous movement (e.g., foot shuffling, hand/arm movements); fidgeting; restlessness; diminished productivity; [crying/tearfulness]; [pacing/purposeless activity]; [immobility]
Affective
Increased wariness; focus on self; irritability; overexcited; anguish; painful and persistent increased helplessness
Physiological
Voice quivering; trembling/hand tremors; increased tension; facial tension; increased pulse; increased perspiration; cardiovascular excitation (s); facial flushing (s); superficial vasoconstriction (s); increased blood pressure (s); twitching (s); increased reflexes (s); urinary urgency (p); decreased blood pressure (p); insomnia; anorexia (s); increased respiration (s)
Cognitive
Preoccupation; impaired attention; difficulty concentrating; forgetfulness; diminished ability to problem-solve; diminished learning ability; rumination; tendency to blame others; blocking of thought; confusion; decreased perceptual field

Sources Of Drugs

Where do medications come from? Historically, drugs were mainly derived from plants (eg, morphine), animals (eg, insulin), and minerals (eg, iron). Now, most drugs are synthetic chemical compounds manufactured in laboratories. Chemists, for example, can often create a useful new drug by altering the chemical structure of an existing drug (eg, adding, deleting, or altering a side-chain). Such techniques and other technologic advances have enabled the production of new drugs as well as synthetic versions of many drugs originally derived from plants and animals. Synthetic drugs are more standardized in their chemical characteristics, more consistent in their effects, and less likely to produce allergic reactions. Semisynthetic drugs (eg, many antibiotics) are naturally occurring substances that have been chemically modified.


Biotechnology is also an important source of drugs. This process involves manipulating deoxyribonucleic acid (DNA) and ribonucleic acid (RNA) and recombining genes into hybrid molecules that can be inserted into living organisms (Escherichia coli bacteria are often used) and repeatedly reproduced. Each hybrid molecule produces a genetically identical molecule, called a clone. Cloning makes it possible to identify the DNA sequence in a gene and produce the protein product encoded by a gene, including insulin and several other body proteins. Cloning also allows production of adequate amounts of the drug for therapeutic or research purposes.

Hepatitis C - Transmission

Parenteral exposure to the hepatitis C virus is the most efficient means of transmission. The majority of patients infected with HCV in Europe and the United States acquired the disease through intravenous drug use or blood transfusion, which has become rare since routine testing of the blood supply for HCV began. The following possible routes of infection have been identified in blood donors (in descending order of transmission risk):
• Injection drug use
• Blood transfusion
• Sex with an intravenous drug user
• Having been in jail more than three days
• Religious scarification
• Having been struck or cut with a bloody object
• Pierced ears or body parts
• Immunoglobulin injection


Very often in patients with newly diagnosed HCV infection no clear risk factor can be identified.
Factors that may increase the risk of HCV infection include greater numbers of sex partners, history of sexually transmitted diseases, and failure to use a condom. Whether underlying HIV infection increases the risk of heterosexual HCV transmission to an uninfected partner is unclear. The seroprevalence of HCV in MSM (men who have sex with men) ranges from about 4 to 8%, which is higher than the HCV prevalence reported for general European populations.
The risk of perinatal transmission of HCV in HCV RNA positive mothers is estimated to be 5% or less (Ohto 1994). Caesarean section has not been shown to reduce transmission. There is no evidence that breastfeeding is a risk factor.
Hemodialysis risk factors include blood transfusions, the duration of hemodialysis, the prevalence of HCV infection in the dialysis unit, and the type of dialysis. The risk is higher with in-hospital hemodialysis vs peritoneal dialysis.
Contaminated medical equipment, traditional medicine rites, tattooing, and body piercing are considered rare transmission routes.
There is some risk of HCV transmission for health care workers after unintentional needle-stick injury or exposure to
other sharp objects.

Nursing Diagnosis and Nursing Intervention for Neonatal Tetanus

Nursing Diagnosis for Neonatal Tetanus
Ineffective breathing pattern related to respiratory muscle fatigue
Imbalanced nutrition, Less than body requirements related to the baby's sucking reflex is inadequate.


Nursing Intervention for Neonatal Tetanus
Nursing Diagnosis I
Ineffective breathing pattern related to respiratory muscle fatigue
Nursing Intervention:
Assess the frequency and pattern of breath
Note the presence of apnea, the frequency change of heart, muscle tone and skin color.
Perform cardiac and respiratory monitoring continuously.
Suction airway as needed.
Give the tactile stimulation immediately after apnea.
Monitor laboratory tests as indicated.
Give oxygenation as indicated.
Give medications as indicated.
Nursing Diagnosis II
Imbalanced nutrition, Less than body requirements related to the baby's sucking reflex is inadequate.
Nursing Intervention:
Assess the maturity of the reflex with respect to feeding, sucking, swallowing and coughing.
Auscultation bowel sounds.
Review the signs of hypoglycemia.
Give appropriate medication electrolyte supplements.
Give parenteral nutrition.
Monitor laboratory tests as indicated.
Make provision of drinking according to tolerance.

Neonatal Tetanus : Definition, Causes and Prevention

Definition of Neonatal Tetanus
Tetanus is a neurological disorder (caused by gram-positive rod Clostridium tetani) which is characterized by increased in muscle tone and muscle spasms. If tetanus occurs in neonates (neonate is a baby of age less than 4 weeks or 28 days) it is called “neonatal tetanus”. Neonatal tetanus is commonly seen in the first 2 weeks of life.


Causes of Neonatal Tetanus
Tetanus is caused by bacteria Clostridium tetani, which is gram-positive rod. Clostridium tetani is a motile and an anaerobic (grows in absence of air or oxygen) organism. Clostridium tetani is worldwide in distribution and found in soil, animal feces, and inanimate objects (at the tip of thorns, iron nails and in many other objects) and sometimes even in human excreta.
The specialty of Clostridium tetani is its ability to form “spores” which are colorless, oval, and look like drumstick or tennis racket. The spores can survive for years (may be decades) in some environment and become vegetative form when the environment is favorable. The spores of Clostridium tetani are resistant to boiling for 20 minutes and also resistant to several disinfectants, which makes it very difficult to remove from environment. But the vegetative forms are easily deactivated by various antibiotics (penicillin, metronidazole etc.) and normal disinfection procedures.
Prevention of Neonatal Tetanus
Neonatal tetanus can be effectively prevented by adapting asceptic techniques during delivery and by conducting delivery in hospitals (institutional delivery). If the delivery is done at home (as is the practice in many developing countries) the umbilical cord should be cut with sterile instrument/blade.
As part of prevention, active immunization of all pregnant women with tetanus toxoid should be done. For the first time pregnancy 2 doses of tetanus toxoid should be administered intramuscularly in the deltoid muscle during 16th to 28th week of pregnancy with at least 4 weeks apart, irrespective of immunization status against tetanus. During subsequent pregnancies, single tetanus toxoid should be administered intramuscularly during 16th to 28th week of pregnancy to prevent neonatal tetanus.
Source : http://nethealthsite.com

ineffective Airway Clearance - Evaluation, Interventions, Documentation

Desired Outcomes/Evaluation
Criteria—Client Will:
• Maintain airway patency.
• Expectorate/clear secretions readily.
• Demonstrate absence/reduction of congestion with breath sounds clear, respirations noiseless, improved oxygen exchange (e.g., absence of cyanosis, ABG results within client norms).
• Verbalize understanding of cause(s) and therapeutic management regimen.
• Demonstrate behaviors to improve or maintain clear airway.
• Identify potential complications and how to initiate appropriate preventive or corrective actions.

Actions/Interventions
NURSING PRIORITY NO. 1. To maintain adequate, patent airway:
• Position head midline with flexion appropriate for age/condition to open or maintain open airway in at-rest or compromised individual.
• Assist with appropriate testing (e.g., pulmonary function/ sleep studies) to identify causative/precipitating factors.
• Suction naso/tracheal/oral prn to clear airway when secretions are blocking airway.
• Elevate head of the bed/change position every 2 hours and prn to take advantage of gravity decreasing pressure on the diaphragm and enhancing drainage of/ventilation to different lung segments (pulmonary toilet).
• Monitor infant/child for feeding intolerance, abdominal distention, and emotional stressors that may compromise
airway.
• Insert oral airway as appropriate to maintain anatomic position of tongue and natural airway.
• Assist with procedures (e.g., bronchoscopy, tracheostomy) to clear/maintain open airway.
• Keep environment allergen free (e.g., dust, feather pillows, smoke) according to individual situation.

NURSING PRIORITY NO. 2. To mobilize secretions:
• Encourage deep-breathing and coughing exercises; splint chest/incision to maximize effort.
• Administer analgesics to improve cough when pain is inhibiting effort. (Caution: Overmedication can depress respirations and cough effort.)
• Give expectorants/bronchodilators as ordered.
• Increase fluid intake to at least 2000 mL/day within level of cardiac tolerance (may require IV) to help liquefy secretions. Monitor for signs/symptoms of congestive heart failure (crackles, edema, weight gain).
• Encourage/provide warm versus cold liquids as appropriate.
• Provide supplemental humidification, if needed (ultrasonic nebulizer, room humidifier).
• Perform/assist client with postural drainage and percussion as indicated if not contraindicated by condition, such as asthma.
• Assist with respiratory treatments (intermittent positivepressure breathing—IPPB, incentive spirometer).
• Support reduction/cessation of smoking to improve lung function.
• Discourage use of oil-based products around nose to prevent aspiration into lungs.

NURSING PRIORITY NO. 3. To assess changes, note complications:
• Auscultate breath sounds and assess air movement to ascertain status and note progress.
• Monitor vital signs, noting blood pressure/pulse changes.
• Observe for signs of respiratory distress (increased rate, restlessness/anxiety, use of accessory muscles for breathing).
• Evaluate changes in sleep pattern, noting insomnia or daytime somnolence.
• Document response to drug therapy and/or development of adverse side effects or interactions with antimicrobials,
steroids, expectorants, bronchodilators.
• Observe for signs/symptoms of infection (e.g., increased dyspnea with onset of fever, change in sputum color, amount, or character) to identify infectious process/promote timely intervention.
• Obtain sputum specimen, preferably before antimicrobial therapy is initiated, to verify appropriateness of therapy.
• Monitor/document serial chest x-rays/ABGs/pulse oximetry readings.
• Observe for improvement in symptoms.

NURSING PRIORITY NO. 4. To promote wellness (Teaching/
Discharge Considerations):
• Assess client’s knowledge of contributing causes, treatment plan, specific medications, and therapeutic procedures.
• Provide information about the necessity of raising and expectorating secretions versus swallowing them, to examine and report changes in color and amount.
• Demonstrate pursed-lip or diaphragmatic breathing techniques, if indicated.
• Review breathing exercises, effective cough, use of adjunct devices (e.g., IPPB or incentive spirometer) in preoperative teaching.

• Encourage/provide opportunities for rest; limit activities to level of respiratory tolerance. (Prevents/lessens fatigue.)
• Refer to appropriate support groups (e.g., stop-smoking clinic, COPD exercise group, weight reduction).
• Instruct in use of nocturnal positive pressure air flow for treatment of sleep apnea. (Refer to NDs disturbed Sleep
Pattern; Sleep Deprivation.)

Documentation Focus
ASSESSMENT/REASSESSMENT
• Related Factors for individual client.
• Breath sounds, presence/character of secretions, use of accessory muscles for breathing.
• Character of cough/sputum.
PLANNING
• Plan of care and who is involved in planning.
• Teaching plan.
IMPLEMENTATION/EVALUATION
• Client’s response to interventions/teaching and actions
performed.
• Attainment/progress toward desired outcome(s).
• Modifications to plan of care.
DISCHARGE PLANNING
• Long-term needs and who is responsible for actions to be taken.
• Specific referrals made.

Nursing Care Plan for Common Dysrhytmias

Normally, the heartbeat begins in the right atrium when the sinoatrial (SA) node, a special group of cells, transmits an electrical signal across the heart. This signal spreads throughout the atria and to the atrioventricular (AV) node. The AV node connects to a group of fibers in

The sinoatrial node is the heart's pacemaker.

the ventricles that conducts the electrical signal and sends the impulse to all parts of the ventricles. This exact route must be followed to ensure that the heart pumps properly.

COMMON DYSRHYTHMIAS

Tachycardias
I. Sinus Tachycardia
a. Sinus node creates rate that is faster than normal (greater than 100)
b. Associated with physiological or psychological stress; medications, such as catecholamines, aminophylline, atropine, stimulants, and illicit drugs; enhanced automaticity; and autonomic dysfunction
II. Atrial Flutter
a. Occurs in the atrium and creates regular atrial rates between 250 and 400. Because AV node cannot keep up with conduction of all these impulses, not all atrial impulses are conducted into the ventricle, causing a therapeutic block at
the AV node.
III. Atrial Fibrillation (AF)
a. Rapid, irregular twitching of the atrial musculature with an atrial rate of 300 to 600 and a ventricular rate of 120 to
200 if untreated
b. Associated with advanced age, valvular heart disease, hyperthyroidism, pulmonary disorder, pulmonary disease,
alcohol ingestion (“holiday heart syndrome”), hypertension, diabetes, CAD, or after open-heart surgery
IV. Paroxysmal Supraventricular Tachycardia (PSVT, also called SVT)
a. Pathways in the AV node or atrium allow an altered conduction of electricity, causing a regular and fast rate of
sometimes more than 150 to 200.
b. Ventricle, sensing the electrical activity coming through the AV node, beats along with each stimulation.
c. Rarely a life-threatening event, but most people feel uncomfortable when PSVT occurs.
V. Ventricular Tachycardia (VT)
a. Rapid heartbeat initiated within the ventricles, characterized by three or more consecutive premature ventricular
beats with elevated and regular heart rate (such as 160 to 240 beats per minute)
b. Heart rate sustained at a high rate causes symptoms such as weakness, fatigue, dizziness, fainting, or palpitations
c. Potentially lethal disruption of normal heartbeat that can degenerate to ventricular fibrillation
VI. Ventricular Fibrillation (VF)
a. Aside from myocardial ischemia, other causes of ventricular fibrillation may include severe weakness of the heart
muscle, electrolyte disturbances, drug overdose, and poisoning.
b. Electrical signal is sent from the ventricles at a very fast and erratic rate, impairing the ability of ventricles to fill
with blood and pump it out, markedly decreasing cardiac output, and resulting in very low blood pressure and loss
of consciousness.
c. Sudden death will occur if VF not corrected.

Bradycardias
I. Sinus Bradycardia
a. Rarely symptomatic until heart rate drops below 50, then fainting or syncope may be reported
b. Causes include hypothyroidism, athletic training, sleep, vagal stimulation, increased intracranial pressure, MI, hypovolemia, hypoxia, acidosis, hypokalemia and hyperkalemia, hyperglycemia, hypothermia, toxins, tamponade, tension pneumothorax, thrombosis (cardiac or pulmonary), and trauma.
c. Medications, such as beta blockers, calcium channel blockers, and amiodarone, also slow the heart rate (AHA, 2005).
II. Sick Sinus Syndrome (SSS)
a. Varity of conditions affecting SA node function, including bradycardia, sinus arrest, sinoatrial block, episodes of
tachycardia, and carotid hypersensitivity
b. Signs and symptoms related to cerebral hypoperfusionc. May be associated with rapid rate (tachycardia) or alternate between too fast and too slow (bradycardia-tachycardia syndrome). A long pause (asystole) may occur between heartbeats, especially after an episode of tachycardia.
III. Heart Blocks
a. First-degree AV block
i. Asymptomatic; usually an incidental finding on electrocardiogram (ECG)
b. Second-degree AV (type I and type II)
i. Usually asymptomatic, although some clients can feel irregularities (palpitations) of the heartbeat, or syncope
may occur, which usually is observed in more advanced conduction disturbances such as Mobitz II AV block

ii. Medications affecting AV node function, such as digoxin, beta blockers, calcium channel blockers, may contribute
c. Third-degree AV block (also called complete heart block)
i. May be associated with acute MI either causing the block or related to reduced cardiac output from bradycardia in
the setting of advanced atherosclerotic CAD ii. Symptomatic with fatigue, dizziness, and syncope and possible loss of consciousness
iii. Can be life-threatening, especially if associated with heart failure

Other Dysrhythmias
I. Premature Atrial Complex (PAC)
a. Electrical impulse starts in the atrium before the next normal impulse of the sinus node.
b. Causes include caffeine, alcohol, and nicotine use, stretched atrial myocardium; anxiety; hypokalemia; and hypermetabolic states (pregnancy), or may be related to atrial ischemia, injury, or infarction.

II. Premature Ventricular Contraction (PVC)
a. Electrical signal originates in the ventricles, causing them to contract before receiving the electrical signal from the atria.
b. PVCs not uncommon and are often asymptomatic.
c. Increase to several per minute may cause symptoms such as weakness, fatigue, dizziness, fainting, or palpitations.
d. Irritability of the heart demonstrated by frequent and or multiple back-to-back PVCs can lead to VF.

Care Settings
Generally, minor dysrhythmias are monitored and treated in the community setting; however, potential life-threatening situations (including heart rates above 150 beats per minute) may require a short inpatient stay.

Nursing Priorities
1. Prevent or treat life-threatening dysrhythmias.
2. Support client and significant other (SO) in dealing with anxiety and fear of potentially life-threatening situation.
3. Assist in identification of cause or precipitating factors.
4. Review information regarding condition, prognosis, and treatment regimen.

Discharge Goals
1. Free of life-threatening dysrhythmias and complications of impaired cardiac output and tissue perfusion.
2. Anxiety reduced and managed.
3. Disease process, therapy needs, and prevention of complications understood.
4. Plan in place to meet needs after discharge.

NURSING DIAGNOSIS: risk for decreased Cardiac Output

Risk factors may include
Altered electrical conduction
Reduced myocardial contractility
Possibly evidenced by
(Not applicable; presence of signs and symptoms establishes an actual diagnosis)
Desired Outcomes/Evaluation Criteria—Client Will
Cardiac Pump Effectiveness
Maintain or achieve adequate cardiac output as evidenced by BP and pulse within normal range, adequate urinary output, palpable pulses of equal quality, and usual level of mentation.
Display reduced frequency or absence of dysrhythmia(s).
Participate in activities that reduce myocardial workload.

ACTIONS/INTERVENTIONS
Dysrhythmia Management
Independent
Palpate radial, carotid, femoral, and dorsalis pedis pulses, noting rate, regularity, amplitude (full or thready), and symmetry.
Document presence of pulsus alternans, bigeminal pulse, or pulse deficit.
Auscultate heart sounds, noting rate, rhythm, presence of extra heartbeats, and dropped beats.
Monitor vital signs. Assess adequacy of cardiac output and tissue perfusion, noting significant variations in BP, pulse
rate equality, respirations, changes in skin color and temperature, level of consciousness and sensorium, and urine
output during episodes of dysrhythmias.
Determine type of dysrhythmia and document with rhythm strip if cardiac or telemetry monitoring is available:
Sinus tachycardia
Sinus bradycardia
Atrial dysrhythmias, such as PACs, atrial flutter, AF, and atrial supraventricular tachycardias (i.e., paroxysmal atrial
tachycardia [PAT], multifocal atrial tachycardia [MAT], SVT)
Ventricular dysrhythmias, such as PVCs and ventricular premature beats (VPBs), VT, and ventricular flutter and VF
Heart blocks
Provide calm and quiet environment. Review reasons for limitation of activities during acute phase.
Demonstrate and encourage use of stress management behaviors such as relaxation techniques; guided imagery;
and slow, deep breathing.
Investigate reports of chest pain, documenting location, duration, intensity (0 to 10 scale), and relieving or aggravating factors. Note nonverbal pain cues, such as facial grimacing, crying, changes in BP and heart rate.
Be prepared to initiate cardiopulmonary resuscitation (CPR), as indicated.
Collaborative
Monitor laboratory studies, such as the following:
Electrolytes
Medication and drug levels
Administer supplemental oxygen, as indicated.
Prepare for and assist with diagnostic and treatment procedures such as EP studies, radiofrequency ablation (RFA), and cryoablation (CA).
Administer medications, as indicated, for example:
Potassium
Antidysrhythmics, such as the following:
Class I drugs:
Class Ia, such as disopyramide (Norpace), procainamide
(Procan SR), quinidine (Cardioquin), and moricizine
(Ethmozine)
Class Ib, such as lidocaine (Xylocaine), phenytoin (Dilantin), tocainide (Tonocard), and mexiletine (Mexitil)
Class Ic, such as flecainide (Tambocor) and propafenone (Rhythmol)
Class II drugs, such as atenolol (Tenormin), propranolol (Inderal), nadolol (Corgard), acebutolol (Sectral), esmolol (Brevibloc), sotalol (Betapace), and bisoprolol (Zebeta)
Class III drugs, such as bretylium tosylate (Bretylol), amiodarone (Cordarone), sotalol (Betapace), ibutilide (Corvert), and dofetilide (Tikosyn)
Class IV drugs, such as verapamil (Calan), nifedipine (Procardia), and diltiazem (Cardizem)
Class V drugs, such as atropine sulfate, isoproterenol (Isuprel), and cardiac glycosides (digoxin [Lanoxin])
Adenosine (Adenocard)
Prepare for and assist with elective cardioversion.
Assist with insertion and maintain pacemaker (external or temporary, internal or permanent) function.
Insert and maintain intravenous (IV) access.
Prepare for surgery, such as aneurysmectomy, CABG, and Maze, as indicated.
Prepare for placement of ICD when indicated.

RATIONALE
Differences in equality, rate, and regularity of pulses are indicative of the effect of altered cardiac output on systemic
and peripheral circulation.
Specific dysrhythmias are more clearly detected audibly than by palpation. Hearing extra heartbeats or dropped beats
helps identify dysrhythmias in the unmonitored client.
Although not all dysrhythmias are life-threatening, immediate treatment may be required to terminate dysrhythmia in the presence of alterations in cardiac output and tissue perfusion.
Useful in determining need and type of intervention required.
Tachycardia can occur in response to stress, pain, fever, infection, coronary artery blockage, valvular dysfunction,
hypovolemia, hypoxia, or as a result of decreased vagal tone or of increased sympathetic nervous system activity
associated with the release of catecholamines. Although it generally does not require treatment, persistent tachycardia may worsen underlying pathology in clients with ischemic heart disease because of shortened diastolic filling time and increased oxygen demands. These clients may require medications.
Bradycardia is common in clients with acute MI (especially anterior and inferior) and is the result of excessive parasympathetic activity, blocks in conduction to the SA or AV nodes, or loss of automaticity of the heart muscle.
Clients with severe heart disease may not be able to compensate for a slow rate by increasing stroke volume; therefore, decreased cardiac output, HF, and potentially lethal ventricular dysrhythmias may occur.
PACs can occur as a response to ischemia and are normally harmless, but can precede or precipitate AF. Acute and chronic atrial flutter or fibrillation (the most common dysrhythmia) can occur with coronary artery or valvular disease and may or may not be pathological. Rapid atrial flutter or fibrillation reduces cardiac output as a result of
incomplete ventricular filling (shortened cardiac cycle) and increased oxygen demand.
PVCs or VPBs reflect cardiac irritability and are commonly associated with MI, digoxin toxicity, coronary vasospasm,
and misplaced temporary pacemaker leads. Frequent, multiple, or multifocal PVCs result in diminished cardiac output
and may lead to potentially lethal dysrhythmias, such as VT or sudden death or cardiac arrest from ventricular flutter or VF. Note: Intractable ventricular dysrhythmias unresponsive to medication may reflect ventricular aneurysm.
Polymorphic VT (torsades de pointes) is recognized by inconsistent shape of QRS complexes and is often related to use of drugs such as procainamide (Pronestyl), quinidine (Quinaglute), disopyramide (Norpace), and sotalol (Betapace).
Reflect altered transmission of impulses through normal conduction channels (slowed, altered) and may be the result of MI, CAD with reduced blood supply to SA or AV nodes, drug toxicity, and sometimes cardiac surgery. Progressing heart block is associated with slowed ventricular rates, decreased cardiac output, and potentially lethal ventricular dysrhythmias or cardiac standstill.
Reduces stimulation and release of stress-related catecholamines, which can cause or aggravate dysrhythmias and vasoconstriction, increasing myocardial workload.
Promotes client participation in exerting some sense of control in a stressful situation.
Reasons for chest pain are variable and depend on underlying cause. However, chest pain may indicate ischemia due
to altered electrical conduction, decreased myocardial perfusion, or increased oxygen need, such as impending or evolving MI.
Development of life-threatening dysrhythmias requires prompt intervention to prevent ischemic damage or death.
Imbalance of electrolytes, such as potassium, magnesium, and calcium, adversely affects cardiac rhythm and contractility.
Reveal therapeutic and toxic level of prescription medications or street drugs that may affect or contribute to presence of dysrhythmias.
Increases amount of oxygen available for myocardial uptake, reducing irritability caused by hypoxia.
Treatment for several tachycardia dysrhythmias, including SVT, atrial flutter, Wolf-Parkinson-White ( WPW) syndrome, AF, and VT, is often carried out as first-line treatment via heart catheterization or angiographic procedures. After rhythm is confirmed with EP study, the client will then often have either an RFA or CA to terminate or disrupt the dysfunctional pattern. Medications may be tried first or added after ablation for increased treatment success.
Correction of hypokalemia may be sufficient to terminate some ventricular dysrhythmias. Note: Potassium imbalance is the number one cause of AF.
Class I drugs depress depolarization and alter repolarization, stabilizing the cell. These drugs are divided into groups a,
b, and c, based on their unique effects.
These drugs increase action potential, duration, and effective refractory period and decrease membrane responsiveness, prolonging both QRS complex and QT interval. This also results in decreasing myocardial conduction velocity and excitability in the atria, ventricles, and accessory pathways.
They suppress ectopic focal activity. Useful for treatment of atrial and ventricular premature beats and repetitive dysrhythmias, such as atrial tachycardias and atrial flutter and AF. Note: Myocardial depressant effects may be potentiated when class Ia drugs are used in conjunction with any drugs possessing similar properties.
These drugs shorten the duration of the refractory period (QT interval), and their action depends on the tissue affected and the level of extracellular potassium. These drugs have little effect on myocardial contractility, AV and intraventricular conduction, and cardiac output. They also suppress automaticity in the His-Purkinje system. Drugs of choice for ventricular dysrhythmias, they are also effective for automatic and re-entrant dysrhythmias and digoxininduced dysrhythmias. Note: These drugs may aggravate myocardial depression.
These drugs slow conduction by depressing SA node automaticity and decreasing conduction velocity through the atria, ventricles, and Purkinje’s fibers. The result is prolongation of the PR interval and lengthening of the QRS complex. They suppress and prevent all types of ventricular dysrhythmias. Note: Flecainide increases risk of druginduced dysrhythmias post-MI. Propafenone can worsen or cause new dysrhythmias, a tendency called the “pro-arrhythmic effect.”
Beta-adrenergic blockers have antiadrenergic properties and decrease automaticity. They reduce the rate and force of cardiac contractions, which in turn decrease cardiac output, blood pressure, and peripheral vascular resistance.
Therefore, they are useful in the treatment of dysrhythmias caused by SA and AV node dysfunction, including SVTs, atrial flutter and AF. Note: These drugs may exacerbate bradycardia and cause myocardial depression, especially when combined with drugs that have similar properties.
These drugs prolong the refractory period and action potential duration, consequently prolonging the QT interval. They decrease peripheral resistance and increase coronary blood flow. They have anti-anginal and anti-adrenergic properties.
They are used to terminate VF and other life-threatening ventricular dysrhythmias and sustained ventricular tachyarrhythmias, especially when lidocaine and procainamide are not effective. Note: Sotalol is a nonselective beta
blocker with characteristics of both class II and class III.
Calcium antagonists, or calcium channel blockers, slow conduction time through the AV node, prolonging PR interval to decrease ventricular response in SVTs, atrial flutter and AF. Calan and Cardizem may be used for bedside conversion of acute AF.
Miscellaneous drugs useful in treating bradycardia by increasing SA and AV conduction and enhancing automaticity.
Cardiac glycosides may be used alone or in combination with other antidysrhythmic drugs to reduce ventricular rate in presence of uncontrolled or poorly tolerated atrial tachycardias or atrial flutter and AF.
First-line treatment for PSVT. Slows conduction and interrupts reentry pathways in AV node. Note: Contraindicated in
clients with second- or third-degree heart block or those with SSS who do not have a functioning pacemaker.
May be used in AF after trials of first-line drugs, such as atenolol, metoprolol, diltiazem, and verapamil, have failed to control heart rate or in certain unstable dysrhythmias to restore normal heart rate or relieve symptoms of heart failure.
Temporary pacing may be necessary to accelerate impulse formation in bradydysrhythmias, synchronize electrical impulsivity, or override tachydysrhythmias and ectopic activity to maintain cardiovascular function until spontaneous pacing is restored or permanent pacing is initiated.
These devices may include atrial and ventricular pacemakers and may provide single chamber or dual chamber pacing. The placement of implantable cardioverter defibrillators (ICDs) is on the rise.
Patent access line may be required for administration of emergency drugs.
Differential diagnosis of underlying cause may be required to formulate appropriate treatment plan. Resection of ventricular aneurysm may be required to correct intractable ventricular dysrhythmias unresponsive to medical therapy.
Surgery such as CABG may be indicated to enhance circulation to myocardium and conduction system. Note: A Maze procedure is an open heart surgical procedure sometimes used to treat refractive AF by surgically redirecting electrical conduction pathways.
This device may be surgically implanted in those clients with recurrent, life-threatening ventricular dysrhythmias unresponsive to tailored drug therapy. The latest generation of devices can provide multilevel or “tiered” therapy, that is, antitachycardia and antibradycardia pacing, cardioversion, or defibrillation depending on how each device is programmed.