Kamis, 05 Mei 2011
CHAPTER I
Dysrhythmias
1. DEFINITIONS
Dysrhythmias are abnormal heart rate that covers the frequency or rhythm disturbances, or both. Dysrhythmias are disturbances of heart electrical system and not the structure of the heart. Dysrhythmias can be identified by analyzing the ECG waves. Dysrhythmias named based on the location and origin of electrical impulses and mechanisms involved.For example, dysrhythmia originating from the sinus node (SA node) and slow frequency is called sinus bradycardia. There are four possible places of origin dysrhythmias: sinus node, atrial, AV node or connection, and the ventricles. Impaired delivery mechanisms that can occur which may include bradycardia, tachycardia, fluter, fibrillation, premature beats, and heart insulation.
2. Etiology
Etiology dysrhythmias in outline can be caused by:
1) Inflammation of the heart, such as rheumatic fever, myocardial inflammation (myocarditis due to infection)
2) disruption of coronary circulation (coronary atherosclerosis or coronary artery spasm, such as myocardial ischemia, myocardial infarction.
3) Because the drug (intoxication among others by digitalis, quinidine, and anti-arrhythmia drugs other.
4) the balance of electrolyte disorders (hyperkalemia, hypokalemia)
5) Interference in the settings that affect the autonomic nervous system and heart rhythm work.
6) psikoneurotik disorders and central nervous
7) metabolic disorders (acidosis, alkalosis)
8) endocrine disorders (hyperthyroidism, hypothyroidism)
9) Disorders of heart rhythm or heart failure
10) cardiac rhythm disorders because of cardiomyopathy or heart tumor
11) cardiac rhythm disturbance due to degeneration disease (heart conduction system fibrosis).
As for the factors that can trigger dysrhythmias, namely:
1) The drugs, especially class IA drugs (quinidine, disopiramid, procainamide) and IC (flekainid, propafenon), digitalis, tricyclic antidepressants, theophylline.
2) Impaired balance of electrolytes and blood gases mainly hypo and hyperkalemia, acidosis.
3) congestive heart trouble: a result of neurohumoral activation.
4) cardiac abnormalities and aritmogenik: Wolf Parkinson White syndrome, and long QT syndrome.
5) Impaired ventilation, infection, anemia, hypotension and shock: superventrikuler tachycardia can occur.
6) thyrotoxicosis cause atrial fibrillation and flutter.
The type Disrirmia, as follows:
1) Dysrhythmias sinus node, comprising:
a) sinus bradycardia
b) Sinus Tachycardia
2) Dysrhythmias atrium, comprising:
a) Premature atrial contraction
b) Paroxysmal atrial tachicardi
c) Atrial Flutter
d) Atrium fibrillation
3) Dysrhythmias ventricle, comprising:
a) Premature ventricular contraction
b) ventricle bigemini
c) ventricle tachicardi
d) ventricle fibrillation
4) Abnormality of delivery, comprising:
a) first-degree AV block
b) second-degree AV block
a. Second-degree AV block type 1
b. Second-degree AV block type 2
c) third degree AV block (total AV block)
d) Asistole ventricle
The cause of congenital heart disease can not be known for certain, but there are several factors that allegedly have an influence on increasing the incidence of congenital heart disease:
1. Prenatal factors:
a) My mother suffered from infectious diseases: Rubella.
b) Mother alcoholism.
c) maternal age over 40 years.
d) My mother suffered from Diabetes Mellitus (DM) who require insulin.
e) Mother taking medicines or herbal tranquilizers.
2. Genetic factors:
a) Children born before suffering from congenital heart disease.
b) Father / Mother suffered from congenital heart disease.
c) chromosome abnormalities such as Down Syndrome.
d) Born with congenital abnormalities of the other.
3. Pathophysiology
1. Sinus node dysrhythmias
a. Sinus bradycardia
Sinus bradycardia may occur because of vagal stimulation, digitalis intoxication, increased intracranial pressure, or myocardial infarction.Sinus bradycardia was also observed in olahraghawan weight, people who are very ill, or people who received treatment (propranolol, reserpin, metildopa), the state hipoendokrin (miksedema, adison disease, panhipopituitarisme), in anorexia nervosa, in hypothermia, and after surgical damage lymph SA.
Characteristics:
• Frequency: 40 to 60 beats per minute
• P wave: precede each QRS complex, PR interval normal
• QRS Complex: usually normal
• delivery: usually normsl
• Rhythm: Regular
b. Sinus tachycardia
Sinus tachycardia (rapid heartbeat) can disebablkan by fever, acute blood loss, anemia, shock, exercise, congestive heart failure, pain, hipermetabolisme circumstances, anxiety, or treatment simpatomimetika parasimpatolitik.
Characteristics:
• Frequency: 100 to 180 beats per minute
• P wave: precede each QRS complex, can be lost in the preceding T wave, PR interval normal
• QRS Complex: usually have a normal duration
• delivery: usually normsl
• Rhythm: Regular
2. Dysrhythmias Atrium
a. Premature Contractions Atrium
Atrium Premature Contractions (PAC = premature atrial contraction) may be due to the atrial muscle irritability kerana caffeine, alcohol, nicotine, which stretched like Atrium myocardium in congestive heart failure, stress atu anxiety, hypokalemia (low potassium levels), injury, infarction, or state hipermetabolik.
Characteristics:
• Frequency: 60 to 100 beats per minute
• P wave: usually has a different configuration with the P wave originating from the SA node. Another place in the atrium has become iritabel (increased automation) and release the impulse before releasing the SA node impulses normally. PR interval may vary with PR interval impulses originating from the SA node.
• QRS complex: can be normal, deviant or absent. When the ventricle has completed phase rep [olarisasi, they can respond to this stimulus from the atrium awal.Hantaran: usually normsl
• Rhythm: regular, except in case of PAC. P waves will occur early in the cycle and usually will not have a complete compensation gap.
b. Atrium paroxysmal tachycardia
Atrium Paoksismal tachycardia (PAT = paroxysmal atrial tachychardia) is characterized by atrial tachycardia awitan sudden and abrupt termination. Can be triggered by emotions, tobacco, caffeine, fatigue, sympathomimetic medications, or alcohol. PAT is usually not associated with organic heart disease. The frequency is very tinggfi can cause angina due to coronary artei pebnurunan charging. Cardiac output will decrease and heart failure can occur.
Characteristics:
• Frequency: 150 to 250 beats per minute
• P wave: ectopic and distorted than the normal P wave, can be found at the beginning of the T wave, shortened PR interval (less than 0.12 seconds)
• Complex QR: usually normal but can experience distortion in case of electrical irregularities
• delivery: usually normal
• Rhythm: Regular
c. Atrium Flutter
Fluter atrium occurs when there is a point focus in the atrium that captures the heart rhythm and make impulse between 250 to 400 times per minute. Character is important in this dysrhythmia is the sealing treatment on the AV node, which prevents the delivery of multiple impulses. Delivery of impulses through the heart sebenartnya still normal, so the comp; Leks QRS unaffected. This is an important sign of this type dysrhythmias, because hantran 1: 1 atrial impulse is released 250 to 400 times per minute would result in ventricular fibrillation, a life-threatening dysrhythmias.
Characteristics:
• Frequency: the frequency of the atrium between 250 to 400 beats per minute
• P wave: no, but was replaced by a sawtooth pattern generated by the focus in the atrium that releases impulses rapidly. This wave is called the wave F.
• QRS complex: normal configuration and time hantarannya also normal.
• T wave: there but can be covered by the wave fluter
• Rhythm: regular or irregular, depending on the type of separator (eg, 2:1, 3:1, or a combination thereof)
d. Atrium fibrillation
Atrial fibrillation (atrial muscle contraction disorganized and uncoordinated) is usually associated with atherosclerotic heart disease, heart valve disease, congestive heart failure, thyrotoxicosis, cor pulmonale, or congenital heart disease.
3. Ventricular dysrhythmias
a. Premature ventricle contraction
Premature ventricular contraction (PVC = premature ventricular contraction) occurs due to increased automation of ventricular muscle cells. PVC commonly caused by digitalis toxicity, hypoxia, hypokalemia, fever, acidosis, exercise, or increased circulating catecholamines.
b. Bigemini ventricle
Bigemini ventricle is usually caused by digitalis intoxication, coronary artery disease, acute MI, and CHF. Bigemini term refers to the condition in which each beat is premature.
c. Ventricle tachycardia
These dysrhythmias caused by increase in myocardial irritability, as in PVC. The disease is usually associated with coronary artery disease and occurs prior to ventricular fibrillation. Ventricular tachycardia is very dangerous and should be regarded as a state of emergency. Patients are usually aware of this fast rhythm and very anxious.
d. Ventricle fibrillation
Are the throbbing ventricular rapid and not effective. In this dysrhythmias heartbeat is muted and not palpable, and no respiration. The pattern is very irregular and can be distinguished from other types of dysrhythmias. Since there is no coordination of heart activity, it can happen cardiac ventricular fibrillation and death if not promptly corrected.
4. Electrical abnormalities
a. Gap-One AV Degrees
Usually associated with organic heart disease or digitalis effect may be due pleh. This is usually seen in patients with inferior wall myocardial infarction heart.
b. Gap AV-Two Degrees
Also be caused by organic heart disease, IM, or digitalis intoxication.This form of insulation resulting in a reduction of heart frequency and usually decrease in cardiac output (cardiac output = volume x frequency sekuncup heart).
c. Gap AV-Three Degrees
Also associated with organic heart disease, digitalis intoxication, and MI. heart frequency is reduced drastically, resulting in decreased perfusion to vital organs. Like the brain, heart, lung, and skin.
5. ASISTOLE ventricle
It will not happen QRS complex. No heart rate, pulse and respiration.Without immediate treatment, ventricular asistole very fatal.
4. CLINIC manifestations
Most manifestations of clients with arrhythmia is not realized, so that was detected during an uncomfortable feeling like a pounding, palpitations, or a heart rate successively increased and the presence of an irregular pulse rhythm. This situation is not too dangerous, if not occur hemodynamic disturbance. But the clinical manifestations in clients with a dangerous arrhythmia is a client to feel chest pain, dizziness, and even more serious situation was found died suddenly possible clients. That's because the supply of blood that contains nutrients and oxygen needed to tissues is inadequate so that the activity / activities disturbed tissue metabolism.
The clinical appearance of the client as follows:
a. Anxiety
b. Nervous
c. tired and weary, and disturbances activity
d. palpitations
e. chest pain
f. vertigo, syncope
g. signs and symptoms of shortness, crakles
h. sign hipoperfus
5. EXAMINATION SUPPORT
a. ECG: shows the pattern of ischemic injury and conduction disturbances. Stating the type / source of dysrhythmia and effect of electrolyte imbalance and cardiac drugs.
b. Monitor Holder: description ECG (24 hours) may be required to determine in which dysrhythmias are caused by specific symptoms when the patient is active (at home / work). It can also be used to evaluate the function of a pacemaker / drug effects antidisritmia.
c. Photo chest: to show an enlarged heart shadow in connection with ventricular dysfunction or valve.
d. Miokardia imaging scan: may show areas of ischemic / myocardial damage that could affect or disrupt the normal conduction of the wall movement and ability to pump.
e. Exercise stress test: exercise can be done to demonstrate that cause dysrhythmias.
f. Electrolytes: increase or decrease in potassium, calcium, and magnesium can cause dysrhythmias.
g. Examination of drugs: can cause cardiac toxicity Abat, a street drug, or allegations of drug interactions, eg digitalis, quinidine, etc..
h. Examination of thyroid: an increase or decrease in serum thyroid levels can cause / increase dysrhythmias.
i. Sedimentation rate: peningggian can indicate an acute inflammatory process / active, eg endocarditis as trigger factors for dysrhythmias.
j. GDA / pulse oximetry: hypoxemia can cause / mengeksasernasi dysrhythmias.
6. MANAGEMENT
a. Critical Massage
b. Anti-arrhythmia drug
c. Installation of temporary pacemaker
d. Handling of using electric shock devices
CHAPTER II
NURSING WITH CASE dysrhythmias
A. ASSESSMENT
1. ACTIVITY / REST
Symptoms: weakness, general fatigue and because of work.
Signs: Changes in frequency of heart / TD with activity / sport.
2. CIRCULATION
Symptoms: Riwatar previous IM / acute (90% -95% had dysrhythmias), cardiomyopathy, GJK, heart valve disease, hypertension.
Signs:
- Change of TD, eg hypertension or hypotension during the period of dysrhythmias.
- Nadi: maybe not regular, eg a strong pulse, pulsus altenan (regular strong beat / weak pulse), pulse bigeminal (irregular pulse of strong / weak beats).
- Pulse deficit (difference between the apical pulse and radial pulse).
- The sound of the heart: irregular rhythm, extra sounds, the pulse decreases.
- Skin: color and humidity changes, eg pale, cyanosis, sweating (heart failure, shock).
- Edema: dependent, general, DVJ (in the presence of heart failure).
- Urine output: decreased if cardiac output decreased weight.
3. EGO INTEGRITY
Symptoms: - Feeling nervous (with tachyarrhythmia), feeling threatened.
- Stressor in connection with medical problems.
Signs: Anxiety, fear, rejected, angry, anxious, crying.
4. FOOD / FLUIDS
Symptoms:
- Loss of appetite, anorexia.
- No tolerance to food (because of medication).
- Nausea / vomiting.
- Changes in body weight
Signs:
- Changes in body weight.
- Edema
- Changes in skin moisture / turgor.
- Breathing krekels.
5. Neuro Sensory
Symptoms: Dizziness, throbbing, headache.
Signs:
- Status of mental / sensory changes, examples of disorientation, confusion, memory loss, changes in speech patterns / consciousness, seizures, coma.
- Changes in behavior, examples of attacks, lethargy, hallucinations.
- Changes in the pupil (equality and reaction to light).
- Loss of deep tendon reflexes with life-threatening dysrhythmias (ventricular tachycardia, severe bradycardia).
6. Pain / Discomfort
Symptoms: Chest pain, mild to severe, which may or may not disappear by biased anti-angina drugs
Signs: Behavioral distraction, anxiety example.
7. BREATHING
Symptoms:
- Chronic lung disease.
- History or tobacco use over and over.
- Short breath.
- Cough (with or without sputum production).
Signs:
- Change the speed / depth of breathing during episodes of dysrhythmia.
- The sound of the breath: the sound of additional (krekels, rhonchi, wheezing) may have showed respiratory complications, such as left heart failure (pulmonary edema) or pulmonary tromboembolitik phenomenon.
8. SECURITY
Signs:
- Fever.
- Redness of the skin (drug reactions).
- Inflammation, erythema, edema (superficial thrombosis).
- Loss of muscle tone / strength.
9. Counseling
Symptoms:
- Examples of family risk factors, heart disease, stroke.
- Use / do not use drugs disresepkan, examples of cardiac medications (digitalis), anti-coagulants (Coumadin) or other drugs are sold freely, eg cough syrups and analgesics containing ASA.
- The failure to memeprbaiki, examples of recurrent dysrhythmias / unable to recover a life-threatening
Considerations:
- DRG shows the average time in care: 3.2 days.
Plan for repatriation:
- Changes in drug use.
B. Nursing Diagnosis
1. Rissiko high against the decline in cardiac output associated with conduction disturbances eliktrikal; decreased myocardial contractility.
2. Lack of knowledge about the causes / treatment of conditions associated with lack of information / incorrect understanding of medical conditions / needs therapy; do not know the source of information; less mengungat
3. Pain associated with tissue ischemia
4. Intolerans activity associated with weakness / fatigue
5. Risk of tissue perfusion changes associated with inadekuat supply oxygen to the tissues.
C. PLANNING AND RATIONAL
1. Diagnosis: High risk due to decreased cardiac output associated with conduction disturbances eliktrikal; decreased myocardial contractility.
Planning and rational:
a) Feel the pulse (radial, carotid, femoral, dorsalis pedis) record the frequency, regularity, amplitude (full / strong) and symmetrical. Note the pulsus alternan, bigeminal pulse, or pulse deficit.
Rational: the frequency difference, similarity and regularity of the pulse shows the effect of cardiac disorders in systemic circulation / peripheral.
b) Auscultation of heart sounds, note the frequency, rhythm. Record Adaiah extra heartbeat, decreased pulse.
Rational: special dysrhythmias more clearly detected with auditory than with palpation. Pendenganaran of extra heart sounds or pulse reduction help identify dysrhythmias in patients with uncontrolled.
c) Monitor vital signs and examine keadekuatan cardiac output / tissue perfusion. Report significant variation in the TD / pulse frequency, similarity, breathing, changes in skin color / temperature, level of consciousness / sensory, and hakuaran urine during episodes of dysrhythmia.
d) Rationale: although not all life-threatening dysrhythmias, treatment is needed quickly to terminate dysrhythmias on the cardiac disorders and tissue perfusion.
e) Provide quiet environment. Assess the reason for limiting activity during the acute phase
f) Rational: reduction in stress due to removal of excitatory and catecholamines, which cause / increase the dysrhythmia and vasoconstriction and increase employment miokardia.
g) Demonstrate / encourage pemnggunaan pengbaturan behavioral stress, eg relaxation techniques, guidance imagination, breath slowly / in
Rational: to increase patient participation in mengekluarkan some sense of control in stressful situations.
h) Prepare / do cardiac pulmonary resuscitation as indicated
Rational: the occurrence of threatening dysrhythmias, life requires intervention to prevent ischemic damage / death.
i) Provide supplemental oxygen as indicated.
Rational: to increase the amount of oxygen to myocardial preparations, which reduce irritability caused by hypoxia.
j) Prepare for / Help planting or automatic cardioverter defibrillator (AICD) if indicated
k) Rational: This device surgically implanted in patients with recurrent life-threatening dysrhythmias, although given the drug therapy carefully.
2. Pain associated with tissue ischemia
Planning and rational:
a) Investigate complaints of chest pain, note awitan and the factor weights and nonverbal clues penurun.Perhatikan inconvenience
b) Rationale: Pain is typically located subternal and can spread keleher and back. But this is different from ischemia myocardial infarction. In this pain may worsen on inspiration, movement or lying down and relieved by sitting up straight / bent
c) Provide a quiet environment and comfort measures eg: change of position, masasage back, warm compresses cold, emotional support
Rational: to lower the patient's physical and emotional discomfort.
d) Give appropriate entertainment activities
e) Rational: to direct attention, provide distraction in the level of individual activity
f) Give the drug as indicated pain
Rational: to relieve pain and inflammatory responses
3. Intolerans activity associated with weakness / fatigue
a) Assess the patient's response to the activity
Rational: It can affect the activity of cardiac output
b) Monitor the frequency of the heart, TD, breathing after activity
Rational: To help determine the degree of cardiac and pulmonary compensation, decreased BP, tachycardia, dysrhythmias and takipneu is indicative of damage tolerance for activity
c) Maintain bed rest during the period of fever and the appropriate indications
Rationale: Increasing the resolution of inflammation during faseakut of pericarditis / endocarditis.
d) Assist patients in the training program activities
Rational: When inflammation / basic condition persists, the patient may be able to perform the desired activity
4. Lack of knowledge about the causes / treatment of conditions associated with lack of information / incorrect understanding of medical conditions / needs therapy; do not know the source of information; less to remember
Planning and rational:
a) Review of normal cardiac function / conduction eliktrikal
Rational: memeberikan basic knowledge to understand individual variation and to understand the reasons for therapeutic intervention
b) Je; askan / emphasize issues specific dysrhythmias and therapeutic measures for patients / people closest
Rational: terus-menerus/baru information can reduce anxiety in connection dnegan ignorance and prepare the patient / person nearby.Education on the nearest person may be important if the patient is elderly, impaired vision or hearing, or unable or interest to learn / follow instructions. Repeated explanations may be necessary, because anxiety and / or new information barriers to prevent / restrict learning.
c) Assist installation / maintain pacemaker function
d) Rational: temporary pacemaker may need to neningkatkan impulse formation or inhibit takidisritmia and ectopic activity in order to maintain cardiovascular function until repaired or races spur spontaneous dikakukan permanent.
e) Encourage the development exercise regularly, avoid excessive exercise. Identify signs / symptoms that require fast activity, eg dizziness, glare, dyspnea, chest pain.
Rational: if dysrhythmias handled properly, normal activity should be done. Training programs are useful in improving cardiovascular health.
5. Risk of tissue perfusion changes associated with inadekuat supply oxygen to the tissues.
Planning and rational:
a) Investigate chest pain, dyspnea suddenly accompanied by Tachypnoea, pleuritik pain, cyanosis pale
Rational: arterial embolism. Affect the heart can occur as a result of valve disease and chronic dysrhythmias.
b) Observations of limb edema, eroitema
Rational: Inactivity / bed rest longer trigger venous stasis, increasing the risk of venous thrombosis formation
c) Observation hematuri
Rational: Indicates kidney embolism
d) Note the left upper abdominal pain
Rational: indicate embolism splenik
REFERENCES
Barbara C. Long. 1996. Medical Surgical Nursing. New York: Pajajaran Press.
Carpenito J.L. 1997. Nursing Diagnosis. Philadelpia: Lippincott J.B.
Carpenito J.L. 1998. Nursing Diagnosis Handbook. Edition 8. Jakarta: EGC.
Doengoes, Marilyn E. 2000. Nursing Care Plans And Documentation.Edition 3. Jakarta: EGC.
Hudack & Galo. 1996. Critical Care. Holistic Approach. VI edition, volume I Jakarta: EGC.
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