What does the P wave measure quizlet?

*Respiratory Tachypnea, shortness of breath (SOB), orthopnea, dyspnea on exertion, hypoxemia, crackles on lung auscultation, wheeze, dry or productive cough

*Cardiac and peripheral vascular Edema, jugular vein distention (JVD), displaced point of maximum impulse (PMI), S3 gallop rhythm, tricuspid and /or mitral regurgitation murmurs, hypotension, decreased mean arterial pressure (MAP), narrow pulse pressure, cool skin and extremities, delayed capillary refill, tachycardia

*Renal Decreased urinary output, oliguria, rising creatinine.

*Gastrointestinal Abdominal distention, ascites, liver engorgement, positive abdominojugular reflex.

*Central nervous Dizziness, decreased sensorium, syncope, fatigue.

*Behavioral/emotional Anxiety, restlessness

Each small block on the graph paper equals 0.04 second, and five small blocks form a large block, which equals 0.2 second. When an ECG waveform moves toward the top of the paper, it is called a positive deflection. When it moves toward the bottom of the paper, it is called a negative deflection.

*The P wave represents the electrical impulse starting in the sinus node and spreading through the atria (atrial depolarization leading to atrial contraction).
*The QRS complex represents ventricular depolarization. Not all QRS complexes have all three waveforms. The Q wave is the first negative deflection after the P wave. The R wave is the first positive deflection after the P wave, and the S wave is the first negative deflection after the R wave. The QRS complex is normally less than 0.10 seconds in duration (2½ small boxes).
*The T wave represents ventricular repolarization or electrical recovery. It follows the QRS complex and is usually in the same direction as the QRS complex. Atrial repolarization also occurs but is not visible on the ECG because it occurs at the same time as the QRS.
*The U wave may or may not be present, and is thought to represent repolarization of the Purkinje fibers; it is, however, sometimes seen in patients with hypokalemia (low potassium levels), hypertension, or heart disease. If present, the U wave follows the T wave and is usually smaller than the P wave. If tall, it may be mistaken for an extra P wave.

Sinus tachycardia occurs when the sinus node creates an impulse at a faster-than-normal rate. Causes may include the following:
Physiologic or psychological stress (e.g., acute blood loss, anemia, shock, hypervolemia, hypovolemia, heart failure, pain, hypermetabolic states, fever, exercise, anxiety)
Medications that stimulate the sympathetic response (e.g., catecholamines, aminophylline, atropine), stimulants (e.g., caffeine, alcohol, nicotine), and illicit drugs (e.g., amphetamines, cocaine, Ecstasy)

Sinus tachycardia often does not cause symptoms. As the heart rate increases, the diastolic filling time decreases, possibly resulting in reduced cardiac output and associated symptoms (refer to Table 17-1). If the rapid rate persists and the heart can no longer compensate for the decreased ventricular filling, the patient may develop acute pulmonary edema or cardiac ischemia.
ECG characteristics are:
Rate: Greater than 100 bpm
Rhythm: Regular
P wave: Present before each QRS and consistent in size and shape
PR interval: Normal
QRS duration: Normal

TREATMENT
Treatment of sinus tachycardia is usually determined by the severity of symptoms and directed at identifying and treating its cause. For example, tachycardia caused by acute blood loss would be treated with IV fluid replacement and blood transfusion.

Atrial fibrillation causes a rapid, disorganized, and uncoordinated electrical activity within the atria. Atrial fibrillation may be transient, starting and stopping suddenly and occurring for a very short time (paroxysmal), or it may be persistent, requiring treatment to terminate the rhythm or to control the ventricular rate. The erratic atrial contraction promotes formation of thrombi within the atria, increasing the risk for an embolic event such as stroke (brain attack). Atrial fibrillation is usually associated with advanced age, valvular heart disease, CAD, hypertension, heart failure, cardiomyopathy, diabetes, hyperthyroidism, pulmonary disease, chronic lung disease, and surgery (especially open heart surgery). Physiological stressors such as hypoxia, infection, and hypoglycemia, as well as caffeine and sympathomimetic drugs are also associated with atrial fibrillation. Sometimes atrial fibrillation occurs in people without any underlying pathophysiology.
People with atrial fibrillation may be asymptomatic. A rapid ventricular response reduces the time for ventricular filling, resulting in a smaller stroke volume. Additionally, loss of the atrial contraction (sometimes referred to as atrial kick) reduces ventricular filling volume and reduces cardiac output by 25%. This leads to symptoms of fatigue and malaise. The shorter time in diastole reduces the time available for coronary artery perfusion, thereby increasing the risk for myocardial ischemia.
ECG characteristics are:
Rate: Atrial rate is 300 to 400, with a variable ventricular response rate (typically rapid)
Rhythm: Irregular
P wave: No discernible P waves; irregular undulating waves may be seen and are referred to as fibrillatory waves
PR interval: Not measurable
QRS duration: Normal

TREATMENT
Treatment of atrial fibrillation depends on its cause and duration and the patient's symptoms, age, and comorbidities. The management of atrial fibrillation includes controlling the ventricular rate and achieving rhythm conversion to sinus rhythm if possible. Electrical cardioversion is indicated for atrial fibrillation that is hemodynamically unstable (Cordina, & Mead, 2008). Because of the high risk for embolization of atrial thrombi, cardioversion of atrial fibrillation that has lasted longer than 48 hours should be avoided unless the patient has received anticoagulants. For atrial fibrillation of acute onset (usually defined as that with an onset within 48 hours), IV adenosine (Adenocard) has been used to achieve cardioversion to sinus rhythm as well as to assist in the diagnosis.

Warfarin is indicated if the patient with atrial fibrillation is at high risk for stroke (i.e., >75 years of age or has hypertension, diabetes, heart failure, or history of stroke). If immediate anticoagulation is necessary, the patient may be placed on heparin until the warfarin level is therapeutic. Pacemaker implantation or catheter ablation is sometimes indicated for patients who are unresponsive to medications. Catheter ablation is an invasive procedure during which high-frequency radio waves are applied to destroy the tissue at the site of the arrhythmia. Ablation procedures are usually performed in electrophysiologic labs and are similar to other types of heart catheterization. During a catheter ablation, long, thin, flexible tubes are placed in the heart via the vascular system. A diagnostic catheter determines where the abnormal tissue that is causing the arrhythmia is located. High-frequency energy is sent into the tissue, creating a lesion or scar. The area is now ablated (destroyed), thus facilitating normal electrical conduction.

Several approaches are effective in preventing the occurrence of postoperative atrial fibrillation, including preoperative administration of a beta blocker or immediate postoperative administration of IV amiodarone

Ventricular tachycardia (VT) is defined as three or more consecutive ventricular beats, occurring at a rate exceeding 100 bpm. The causes are similar to those of PVC. Ventricular tachycardia is usually associated with CAD and may precede ventricular fibrillation. Untreated ventricular tachycardia can deteriorate into ventricular fibrillation, a lethal arrhythmia.

The patient can experience a range of symptoms related to decreased cardiac output, such as hypotension or syncope, pulselessness, and unresponsiveness. Some patients may be asymptomatic.
ECG characteristics are:
Rate: 100-250 bpm
Rhythm: Regular
P wave: Usually not visible; if visible are not associated with the QRS complex (called dissociation).
PR interval: None
QRS duration: Greater than 0.12 seconds

The patient's tolerance for this rapid rhythm depends on the ventricular rate and underlying disease. Several factors determine the initial treatment, including the following: identifying the rhythm as monomorphic (having a consistent QRS shape and rate) or polymorphic (having varying QRS shapes and rhythms); determining the existence of a prolonged QT interval before the initiation of VT; and ascertaining the patient's heart function. If the patient is stable, continuing the assessment, especially obtaining a 12-lead ECG, may be the only action necessary. Amiodarone administered IV is the antiarrhythmic medication of choice for a stable patient with VT. Cardioversion is the treatment of choice for monophasic VT in a symptomatic patient. Atrial fibrillation should be suspected as the cause of a wide complex tachycardia with an irregular rhythm, and it should be treated appropriately.

Torsades de pointes (Fig. 17-14) is a polymorphic VT usually preceded by a prolonged QT interval (Sommargren & Drew, 2007). Risk factors for torsades de pointes are described in Box 17-5. Because this rhythm is likely to cause the patient to deteriorate and become pulseless, immediate treatment is usually required. Magnesium has frequently been used to treat torsades, but its use has not been proven effective. Any type of VT in a patient who is unconscious and without a pulse is treated in the same manner as ventricular fibrillation: immediate defibrillation is the action of choice.

Ventricular fibrillation is a rapid, disorganized ventricular rhythm that causes ineffective quivering of the ventricles. No atrial activity is seen on the ECG. Causes of ventricular fibrillation are the same as for VT; it may also result from untreated or unsuccessfully treated VT.

Clinical manifestations include absence of an audible heartbeat, a palpable pulse, and respirations. Cardiac arrest and death are imminent.
ECG characteristics are:
Rate: Often cannot be determined, but is greater than 220 bpm
Rhythm: Irregular
P wave: Not visible
PR interval: Not visible
QRS duration: Not visible

TREATMENT
Treatment of choice is immediate defibrillation if available, immediate cardiopulmonary resuscitation (CPR), and activation of emergency services. After the initial defibrillation, five cycles of CPR, alternating with a rhythm check and defibrillation, are used to convert ventricular fibrillation to an electrical rhythm that produces a pulse. Vasoactive medications (epinephrine, vasopressin, or both) should be administered as soon as possible after the second rhythm check (immediately before or after the second defibrillation). Antiarrhythmic medications (amiodarone, lidocaine, or possibly magnesium) should be administered as soon as possible after the third rhythm check (immediately before or after the third defibrillation). Once the patient is intubated, CPR should be administered continuously with one breath every 6 to 8 seconds, not in cycles of 30 compressions to two ventilations, and the rhythm check and medication administration should occur every 2 minutes. In addition, underlying and contributing factors are identified and eliminated throughout the event

Cardioversion and defibrillation are used to treat tachyarrhythmias by delivering an electrical current that depolarizes a critical mass of myocardial cells. When the cells repolarize, the sinus node is usually able to recapture its role as the heart's pacemaker. One major difference between cardioversion and defibrillation is the timing of the delivery of electrical current. In cardioversion, the delivery of the electrical current is synchronized with the patient's electrical events; in defibrillation, the delivery of the current is unsynchronized.

Defibrillation is used in emergency situations as the treatment of choice for ventricular fibrillation and pulseless VT. Defibrillation is not used on patients who are conscious or have a pulse. It has been established that early defibrillation is the major determinant of survival in cardiac arrest (Field, 2008).
The electrical voltage required to defibrillate the heart is usually greater than that required for cardioversion and may cause more myocardial damage. Defibrillators are classified as monophasic or biphasic. Monophasic defibrillators deliver current in only one direction and require increased energy loads. Newer biphasic defibrillators deliver the electrical charge to the positive paddle, which then reverses back to the originating paddle. The recommended energy levels for defibrillation vary according to the type of waveform and the manufacturer of the defibrillator (Finamore & Turris, 2008). Following defibrillation, CPR is immediately initiated if a perfusable rhythm was not initiated, and other advanced life support treatments are begun. This treatment with continuous CPR, medication administration, and defibrillation continues until a stable rhythm resumes or until it is determined that the patient cannot be revived.

The implantable cardioverter defibrillator (ICD) is a device that detects and terminates life-threatening episodes of tachycardia or fibrillation. ICDs are used for patients who have survived sudden cardiac death syndrome, usually caused by ventricular fibrillation, or have experienced symptomatic ventricular tachycardia. Other people at risk of sudden cardiac death include those with dilated cardiomyopathy, hypertrophic cardiomyopathy, arrhythmogenic (capable of inducing an arrhythmia) right ventricular dysfunction, and prolonged QT syndrome. In addition, patients with moderate to severe left ventricular dysfunction, with or without nonsustained VT, are at high risk for cardiac arrest; therefore, prophylactic implantation may be indicated. ICDs may also be implanted in patients with symptomatic, recurrent, medication-refractory atrial fibrillation.

A pacemaker is an electronic device that delivers electrical stimulation to the heart to regulate the heart rate when a patient has a slower-than-normal heart rate or conduction disturbance. They may also be used to control some tachyarrhythmias or to treat advanced heart failure that does not respond to medication. Pacemakers may be temporary or permanent. Temporary pacemakers may be transvenous, transcutaneous, or epicardial.
Pacemaker Design and Types

Pacemakers consist of two components: an electronic pulse generator and pacemaker electrodes, or leads. The generator contains the energy source that determines the rate (measured in bpm) and the strength or output (measured in milliamperes [mA]) of the electrical stimulus delivered to the heart. The generator can be programmed to detect the heart's intrinsic electrical activity and to cause an appropriate response; this component of pacing is called sensitivity and is measured in millivolts (mV). Leads can be threaded through a major vein into the right ventricle (endocardial leads), or they can be lightly sutured onto the outside of the heart and brought through the chest wall during open heart surgery (epicardial wires). The endocardial leads may be temporarily placed with catheters through a great vessel (transvenous wires), usually guided by fluoroscopy. The endocardial and epicardial wires are connected to a temporary external generator.
Endocardial leads may also be placed permanently, usually through the external jugular vein, and connected to a permanent generator. The generator is implanted in a subcutaneous pocket created in the pectoral region below the clavicle (Fig. 17-25). The procedure usually takes about 1 hour, and it is performed in a cardiac catheterization laboratory using a local anesthetic. Batteries need replacement after approximately 10 years; and battery replacement is usually performed using a local anesthetic.
If a patient suddenly develops a symptomatic bradycardia, emergency pacing may be started with transcutaneous pacing. Large pacing ECG electrodes (pads) are placed on the patient's chest and back. The electrodes are connected to the temporary pacemaker generator (Fig. 17-26). Because the impulse must travel through the patient's skin and tissue before reaching the heart, transcutaneous pacing can cause significant discomfort and is intended to be used only in emergencies. If the patient is alert, sedation and analgesia may be administered.

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