320 likes | 338 Views
CCU Competency Module 1. 2013. Introduction. This module will include key points in the following areas. These areas were chosen based on identified opportunities for quality improvement. Antiarrhythmic Pharmacology Hemodynamics Pulmonary Assessment and Treatment.
E N D
Introduction • This module will include key points in the following areas. These areas were chosen based on identified opportunities for quality improvement. • Antiarrhythmic Pharmacology • Hemodynamics • Pulmonary Assessment and Treatment
Several antiarrhythmic medications work on the action potential of the purkinje fibers (myocardial cells in the ventricles). The action potential is based on the movement of key electrolytes across the cell membrane resulting in contraction and relaxation of the myocardium.
The action potential is associated with the waves we record on the ECG and monitor. • Phase 0: Rapid depolarization • SodiumInflux • Sodium channel • Correlates with the beginning of QRS complex • Phase 1: Brief, rapid initiation of repolarization CNEA / Key Choice
Phase 2: Slowing of the repolarization • Calcium Influx • Calcium channel • Correlates with ST segment • Phase 3: Sudden acceleration in the rate of repolarization • Potassium Efflux • Potassium Channel • Correlates with T wave • Phase 4: Resting membrane potential CNEA / Key Choice
Classification of Arrhythmic Medications • Class I – Sodium channelblockers (Impacts Phase I of the Action Potential) • IA:Quinidine, Procainamide, Disopyramide • IB: Lidocaine, Mexiletine, Tocainide • IC: Flecainide, Propafenone • Class II – Betablockers(Does not impact the Action Potential) • Propranolol, Metoprolol, Atenolol, Bisoprolol • Class III – Potassium channel blockers(Impacts Phase III of the Action Potential) • Amiodarone, Dronedarone, Ibutalide, Dofetilide, Sotalol • Class IV – Calcium channel blockers(Impacts Phase II of the Action Potential) • Verapamil, Diltiazem
Calcium Channel Blockers and Beta Blockers Calcium channel blockers and beta blockers are considered antiarrhythmic medications but they are also used for other purposes. Beta blockers do not work directly on the cardiac action potential but rather work by blocking the sympathetic nervous system. Beta blockers and calcium channel blockers are generally considered safer than the Class I and Class III antiarrhythmic agents. In atrial fibrillation, beta blockers and calcium channel blockers can be used for rate control. They are not given to convert the patient to sinus rhythm. Calcium channel blockers are more effective than beta blockers in slowing conduction through the AV node and this is why diltiazem is so often used as the preferred drug in atrial fibrillation with RVR. Only two calcium channel blockers have an impact on cardiac conduction. These are verapamil and diltiazem. All the calcium channel blockers that end in “ine” (amlodipine) do not have an impact on cardiac conduction.
Class I and Class III Antiarrhythmic Agents • Class I antiarrhythmics work on Phase 0 of the cardiac action potential and therefore affect ventricular depolarization. • This means class I antiarrhythmics have the potential to widen the QRS and thus indirectly prolong the QT interval. • Class III antiarrhythmics work on Phase III of the cardiac action potential and therefore affect ventricular repolarization. • This means the T wave is affected (T wave represents ventricular depolarization) and thus the QT is directly prolonged.
Class III Agents • Class III agents are more common in CCU and will be the focus of the remainder of this section. • Ibutilide (Corvert) • IV only • Used to convert atrial fibrillation or flutter to NSR • Dofetilide (Tikosyn) • PO only • Used to convert atrial fibrillation or flutter • Used for rhythm control in patients with atrial fibrillation or flutter (maintenance therapy to keep patient in SR)
Class III Agents continued • Sotalol (Betapace) • Class III agent and also has beta blocker effect • IV or PO • Used for life threatening ventricular arrhythmias • Used for rhythm control in patients with atrial fibrillation or flutter (maintenance therapy to keep patient in SR) • Amiodarone • Class III agent but also has Class I effects, as well as calcium channel blocker and beta blocker effects • IV or PO • Used for ventricular arrhythmias • Used to convert atrial arrhythmias (unlabed) • Used for rhythm control (maintain NSR) in patients with atrial fibrillation or flutter (unlabed) • Dronedarone (Multaq) • Similar to amiodarone • PO only • Used for rhythm control in patients with atrial fibrillation • Contraindicated in permanent atrial fibrillation • Contraindicated in heart failure
Key Nursing Considerations • All Class III antiarrhythmics prolong the QT interval and increase the risk of Torsades de Pointes (polymorphic VT) • Monitoring of the QTc is a priority. • Notify physician or APN of QT or QTc prolongation particularly during initiation of dofetilide or sotalol therapy. • Monitoring of electrolytes is also important. Hypokalemia, hypomagnesemia, and hypocalcemia can all prolong the QT. • Sotalol (Betapace) • Many patients require inpatient initiation due to high risk features. • During initiation in hospital the QTc should be monitored 2 to 4 hours after each dose. • Dose must be adjusted for renal insufficiency. • Dose adjustments are made gradually (3 days between adjustments) to allow for steady states and QTc assessment. • Beta blocker component increases risk for bradycardia and hypotension.
Key Nursing Considerations • Ibutilide (Corvert) • Potassium level must be assessed prior to administration because hypokalemia prolongs repolarization and increases risk of Torsades de Pointes • Medication should be given over 10 minutes • May cause monomorphic VT in addition to Torsades de Pointes • Review hospital policy prior to administration • Dofetilide (Tikosyn) • Must be initiated in the hospital setting due to QTc prolongation. Patients must be monitored for minimum of 3 days or for a minimum of 12 hours after cardioversion (whichever is greater). • Do not hold medication if patient converts to sinus rhythm unless ordered. • QTc must be measured after initial dose and the dose decreased if QT prolongation occurs. • QTc interval assessment should be performed as ordered on the Tikosyn order set. • Dose must be decreased if there is renal insufficiency. • Give medication at the exact times as ordered.
Key Nursing Considerations • Amiodarone • Although it prolongs the QT, it is the least likely of the agents to cause Torsades de Pointes. • Associated with extra cardiac side effects (i.e. interstitial pneumonitis) the risk for these effects is increased with higher doses and longer duration of therapy. • Has a vasodilator effect and may cause hypotension. Slow the rate if hypotension or bradycardia occurs. • Associated with phlebitis, and therefore the more proximal or central the IV access the better. An in-line filter is recommended. Peripheral concentrations should not exceed 2mg/ml. • Not compatible with IV heparin. • Give with food to avoid GI upset. • Dronedarone (Multaq) • Worse outcomes occur when used in patients who continue in atrial fibrillation (permanent) and when used in patients with current or recent decompensated heart failure. • Give with food to avoid GI upset.
For Your Portfolio • Your choice (select one): • Show evidence of CCRN, PCCN, or CHFN certification. • Review an evidence based journal article on an aspect of antiarrhythmic pharmacology and summarize 2 things you learned from the article that can impact patient care. • Review one of the Class III antiarrhythmics in Lexicomp and summarize 2 clinically relevant pieces of information not covered in this module. • Show CE certificate from February 2013 Patient Education Workshop that focused on patient education related to medication therapy. • Use the worksheet in your competency packet or download the competency packet at https://www.dropbox.com/sh/ez02n2v0ueryodw/SNuyZEGZhb
Learning Content • For this section please go to www.aacn.org. This is the home page for the American Association of Critical Care Nurses. • Go to the Practice Alert link (under the Clinical Practice section on the home page). • Read the following two practice alerts • Pulmonary artery pressure measurement • Noninvasive blood pressure monitoring
For Your Portfolio • Summarize two things you learned from the AACN Practice Alerts that you will incorporate into practice. • Also - Your choice: • Show evidence of CCRN, PCCN, or CHFN certification. • Attend a Heart Center Clinical Practice Committee Meeting. • Read an evidence based journal article on hemodynamics and summarize 2 things you learned that can be incorporated into practice. • Show certificate for the Beyond the Core Class • 10 Key Patient Assessment Skills (3/18/2013 or 9/23/2013) • Ask Rhonda Fleischman, Cindy Webner, or Karen Marzlin to observe you perform a square wave test on patient with an arterial line or PA catheter. Identify the results of the square wave test as normal, overdamped, or underdamped. • Use the worksheet in your competency packet or download the competency packet at https://www.dropbox.com/sh/ez02n2v0ueryodw/SNuyZEGZhb
Important Assessment Criteria for All Patients • An accurate respiratory rate should be counted and documented on all patients. Tachypnea is an abnormal assessment finding. • Increased work of breathing is an ominous sign. • Increased work of breathing is a reportable condition. • Patients with an increased work of breathing need ventilatory support. • BiPAP is a noninvasive method for providing ventilatory support and decreasing the work of breathing.
Blood Gas Assessment • When a blood gas is obtained in a patient who is hypoxemic, a key priority is to determine if the patient is in ventilatory failure. • Ventilatory failure results in an elevated PaCO2 on the arterial blood gas. Ventilatory failure is treated by supporting ventilation. Oxygen therapy does not correct inadequate ventilation. Options for treating ventilatory failure include: • BiPAP (not CPAP) • Intubation and mechanical ventilation • Increase in respiratory rate or tidal volume in a patient already on a ventilator * Some patients with COPD may live with a chronically elevated PaCO2. These patients compensate for their respiratory acidosis and develop a normal pH.Decompensation in these patients is recognized by a pH that is no longer compensated. • If the PaCO2 is normal this indicates the patient is adequately ventilating. If the patient is hypoxemic with a normal PaCO2 then oxygenation can be improved by increasing FIO2 or adding pressure (CPAP).
Difference Between CPAP and BiPAP • CPAP and BiPAP are both non invasive methods to support the respiratory system • CPAP is continuous positive airway pressure: • The patient is breathing spontaneously at a higher level of pressure (for example 8 or 10 cmH2O) throughout the respiratory cycle. • The added pressure from CPAP is beneficial in different clinical circumstances. Two of the common reasons for CPAP include: • Provide pressure to keep the airway open during sleep and prevent obstructive sleep apnea. • Provide pressure to help drive oxygen across the alveolar membrane. • Hypoxemia is frequently due to a barrier of the diffusion of oxygen across the alveolar capillary membrane. • This barrier can be caused by fluid (pulmonary edema) or exudate (pneumonia). • There are two ways to help drive oxygen across the membrane: 1) increase FIO2 (which in turn increases the oxygen content in the alveoli and creates a higher gradient between the alveolar oxygen content and the oxygen content in the pulmonary capillary; and 2) add pressure (i.e. CPAP) to help drive the oxygen across the alveolar membrane.
Difference Between CPAP and BiPAP • CPAP can be used to treat oxygenation failure, as long as the reason for the patient’s hypoxemia is not due to ventilatory failure. • CPAP does not correct ventilatory failure. • Ventilatory failure is identified by increased work of breathing or by an elevated PaCO2 on blood gas. • When a patient is in respiratory failure due to ventilatory failure, BiPAP is a potential treatment solution. • BiPAP provides two levels of pressure support. An inspiratory pressure and an expiratory pressure. The higher inspiratory pressure helps to support ventilation. • BiPAP is effective in decreasing the work of breathing. • Initial settings for BiPAP are typically 12 cmH2O for the inspiratory pressure and 6 cmH20 for the expiratory pressure. • BiPAP can only be used if the patient is able to maintain his or her airway. If a patient is significantly hemodynamcially compromised, intubation and mechanical ventilation are preferred to mange ventilation. • BiPAP is also sometimes used in palliative care to decrease work of breathing.
IN SUMMARY: Ventilation vs Oxygenation When evaluating pulmonary status remember to evaluate both oxygenation and ventilation. This will help you better understand how to assist the patient. • Oxygenation Problem • Evaluated by oxygen saturation or PaO2 on arterial blood gas • Treated by increasing oxygen (FiO2) or by adding pressure (CPAP or increased PEEP if on a ventilator) • Ventilation Problem • Evaluated by PaCO2 on blood gas; also evaluated during physical assessment by decreased respiratory rate or inadequate depth of each breath (tidal volume) • Treated by increasing respiratory rate or tidal volume. This may mean: • Adding BiPAP • Reversing sedation • Bagging patient or intubating and ventilating • Increasing rate or tidal volume on ventilator
Sedation in Mechanically Ventilated Patients Patients who are intubated and mechanically ventilated need both sedation and analgesia. Sedation should be administered to achieve a predetermined goal. The goal for most patients should be a patient who awakens to verbal stimuli or gentle touch, and is able to follow commands; but then is able to easily drift back off to sleep. This correlates with a SAS sedation score of 3. Some patients – like those receiving therapeutic hypothermia require a deeper level of sedation. The SAS goal in these patients is a score of 2. Non benzodiazepines (i.e. propofol) are preferred for sedation to reduce the risk of delirium.
Analgesia in the Mechanically Ventilated Patient Analgesia should be administered in conjunction with sedation. Adequate pain control is a priority before sedation to reduce the amount of required sedation and reduce the risk for delirium. Short acting opioids are used for analgesia in most mechanically ventilated patients. Non narcotic medications such a acetaminophen can / should be used to supplement opioids. This is another strategy to decrease the amount of medications that increase the risk for delirium.
Barotrauma(caused by excessive pressure) • Volutrauma(caused by excessive volume) • Ateletrauma(caused by low volume resulting in repetitive opening and closing of distal lung units) • Biotrauma(caused by biochemical mediators released in response to mechanical ventilation) • Ventilator associated pneumonia • Delirium • Complications of immobility • DVT • Skin breakdown Complications in green are reduced by evidenced based nursing care!! Complications of Mechanical Ventilation
A level of PEEP is a set on the ventilator as ordered. A low level of PEEP (i.e. 5 to 10 cmH2O ) prevents the alveoli from collapsing during expiration but does not open aveoli that are already collapsed. PEEP can be increased as needed to improve oxygenation. This works by increasing the driving pressure of oxygen across the alveolar capillary membrane. All positive pressure ventilation decreases venous return to the heart (preload). PEEP further decreases venous return to the heart. This reduction in preload can result in hypotension if the patient does not have an adequate circulating volume. Another potential complication of PEEP is barotrauma to the alveoli from increased pressure. The optimal level of PEEP is considered to be the level at which the patient is well oxygenated and yet free of complications of PEEP. Understanding PEEP (Positive End Expiratory Pressure)
Understanding Auto PEEP • Auto PEEP is a potential complication that can occur during mechanical ventilation when • patients do not have enough time during expiration to exhale lung volume. • In the picture below, inspiration is above baseline and expiration is below • baseline. Inspiration is positive above baseline during mechanical ventilation because the • patient is receiving positive pressure ventilation. • As depicted below expiration is not long enough for the patient to return • to baseline and the next inspiration begins with air still trapped in the alveoli. • Respiratory therapy can utilize this type of waveform analysis to detect auto peep. • Auto peep increases the work of breathing and can cause hypotension.
Reason: Conversion to positive pressure ventilation and / or the addition of increase in PEEP (decreases preload) • Solution: Assure adequate circulating fluid volume • Reason: Blood pressure response to sedation or analgesia • Solution: Titrate sedation / analgesia • Reason: Development of auto PEEP • Solution: Ventilator settings need changed to increase expiration time • Reason: Tension Pneumothorax (air in pleural space; collapse of lung; no means of air escape) • Solution: Chest tube is required • NOTE: Tension pneumothorax is diagnosed by diminished to absent lung sounds on affected side. Potential Reasons for Hypotension with Mechanical Ventilation
For Your Portfolio • Your choice (select one): • Show evidence of CCRN, PCCN, or CHFN certification. • Review an evidence based journal article on an aspect of ventilator management and summarize 2 things you learned from the article that can impact patient care. • Present a case example of a patient you cared for a patient on mechanical ventilation. Include clinical information and key nursing care you provided demonstrating one or more areas of competency in the care of a mechanically ventilated patient. • Show CE certificate for the Beyond the Core Class • Important Nursing Considerations in the Mechanically Ventilated Patient from Friday, April 5thor Monday, October 21st. • Use the worksheet in your competency packet or download the competency packet at https://www.dropbox.com/sh/ez02n2v0ueryodw/SNuyZEGZhb
Thank you for your commitment to excellence in CCU practice! Please see Rhonda Fleischman for any questions.