Transcript Class III Agents

CCU
Competency
Module 1
2013
• This module will include key points in the following
areas. These areas were chosen based on identified
opportunities for quality improvement.
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Antiarrhythmic Pharmacology
Hemodynamics
Pulmonary Assessment and Treatment
Introduction
Antiarrhythmic Pharmacology
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.
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The action potential is associated with the
waves we record on the ECG and monitor.
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Phase 0: Rapid depolarization
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Sodium Influx
Sodium channel
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Correlates with the beginning of QRS complex
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Phase 1: Brief, rapid initiation of repolarization
CNEA / Key Choice
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Phase 2: Slowing of the repolarization
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Calcium Influx
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Calcium channel
Correlates with ST segment
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Phase 3: Sudden acceleration in the rate of repolarization
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Potassium Efflux
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Potassium Channel
Correlates with T wave
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Phase 4: Resting membrane potential
CNEA / Key Choice
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Class I – Sodium channel blockers (Impacts Phase I of the Action Potential)
IA:Quinidine, Procainamide, Disopyramide
– IB: Lidocaine, Mexiletine, Tocainide
– IC: Flecainide, Propafenone
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Class II – Betablockers (Does not impact the Action Potential)
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Class III – Potassium channel blockers (Impacts Phase III of the Action Potential)
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Propranolol, Metoprolol, Atenolol, Bisoprolol
Amiodarone, Dronedarone, Ibutalide, Dofetilide, Sotalol
Class IV – Calcium channel blockers (Impacts Phase II of the Action Potential)
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Verapamil, Diltiazem
Classification of Arrhythmic Medications
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Calcium channel blockers and beta blockers are considered antiarrhythmic medications
but they are also used for other purposes.
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Beta blockers do not work directly on the cardiac action potential but rather work by
blocking the sympathetic nervous system.
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Beta blockers and calcium channel blockers are generally considered safer than the Class
I and Class III antiarrhythmic agents.
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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.
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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.
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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.
Calcium Channel Blockers and Beta Blockers
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Class I antiarrhythmics work on Phase 0 of the cardiac action potential and
therefore affect ventricular depolarization.
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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.
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This means the T wave is affected (T wave represents ventricular depolarization) and
thus the QT is directly prolonged.
Class I and Class III Antiarrhythmic Agents
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Class III agents are more common in CCU and will be the focus of the
remainder of this section.
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Ibutilide (Corvert)
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IV only
Used to convert atrial fibrillation or flutter to NSR
Dofetilide (Tikosyn)
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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
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Sotalol (Betapace)
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Amiodarone
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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)
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)
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Similar to amiodarone
PO only
Used for rhythm control in patients with atrial fibrillation
Contraindicated in permanent atrial fibrillation
Contraindicated in heart failure
Class III Agents continued
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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.
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Sotalol (Betapace)
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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
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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
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Dofetilide (Tikosyn)
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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
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Amiodarone
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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.
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Key Nursing Considerations
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Your choice (select one):
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Show evidence of CCRN, PCCN, or CHFN certification.
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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.
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Review one of the Class III antiarrhythmics in Lexicomp and summarize 2
clinically relevant pieces of information not covered in this module.
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Show CE certificate from February 2013 Patient Education Workshop that
focused on patient education related to medication therapy.
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Use the worksheet in your competency packet or download the
competency packet at
https://www.dropbox.com/sh/ez02n2v0ueryodw/SNuyZEGZhb
FOR YOUR PORTFOLIO
Hemodynamics
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For this section please go to www.aacn.org. This is the home page
for the American Association of Critical Care Nurses.
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Go to the Practice Alert link (under the Clinical Practice section on
the home page).
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Read the following two practice alerts
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Pulmonary artery pressure measurement
Noninvasive blood pressure monitoring
Learning Content
Summarize two things you learned from the AACN Practice
Alerts that you will incorporate into practice.
• Also - Your choice:
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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
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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
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FOR YOUR PORTFOLIO
Pulmonary Assessment and Treatment
• 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.
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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.
Important Assessment Criteria for All Patients
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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.
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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
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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.
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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).
Blood Gas Assessment
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CPAP and BiPAP are both non invasive methods to support the respiratory system
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CPAP is continuous positive airway pressure:
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The patient is breathing spontaneously at a higher level of pressure (for example 8 or 10
cmH2O) throughout the respiratory cycle.
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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.
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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.
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Difference Between CPAP and BiPAP
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CPAP can be used to treat oxygenation failure, as long as the reason for the patient’s
hypoxemia is not due to ventilatory failure.
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CPAP does not correct ventilatory failure.
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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.
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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.
Difference Between CPAP and BiPAP
When evaluating pulmonary status remember to evaluate both oxygenation and
ventilation. This will help you better understand how to assist the patient.
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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)
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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:
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Adding BiPAP
• Reversing sedation
• Bagging patient or intubating and ventilating
• Increasing rate or tidal volume on ventilator
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IN SUMMARY: Ventilation vs Oxygenation
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Patients who are intubated and mechanically ventilated need both
sedation and analgesia.
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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.
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Some patients – like those receiving therapeutic hypothermia require a
deeper level of sedation. The SAS goal in these patients is a score of 2.
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Non benzodiazepines (i.e. propofol) are preferred for sedation to reduce
the risk of delirium.
Sedation in Mechanically Ventilated Patients
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Analgesia should be administered in conjunction with sedation.
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Adequate pain control is a priority before sedation to reduce the
amount of required sedation and reduce the risk for delirium.
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Short acting opioids are used for analgesia in most mechanically
ventilated patients.
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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.
Analgesia in the Mechanically Ventilated Patient
Barotrauma (caused by excessive pressure)
• Volutrauma (caused by excessive volume)
• Ateletrauma (caused by low volume resulting in repetitive opening and
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closing of distal lung units)
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Biotrauma (caused by biochemical mediators released in response to
mechanical ventilation)
Ventilator associated pneumonia
• Delirium
• Complications of immobility
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DVT
Skin breakdown
Complications in green
are reduced by evidenced
based nursing care!!
Complications of Mechanical Ventilation
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A level of PEEP is a set on the ventilator as ordered.
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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.
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PEEP can be increased as needed to improve oxygenation. This works by increasing the
driving pressure of oxygen across the alveolar capillary membrane.
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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.
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Another potential complication of PEEP is barotrauma to the alveoli from increased
pressure.
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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)
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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.
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Reason: Conversion to positive pressure ventilation and / or the
addition of increase in PEEP (decreases preload)
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Reason: Blood pressure response to sedation or analgesia
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Solution: Titrate sedation / analgesia
Reason: Development of auto PEEP
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Solution: Assure adequate circulating fluid volume
Solution: Ventilator settings need changed to increase expiration time
Reason: Tension Pneumothorax (air in pleural space; collapse of lung;
no means of air escape)
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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
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• Your choice (select one):
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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 5th or Monday, October 21st.
• Use the worksheet in your competency packet or download the
competency packet at
https://www.dropbox.com/sh/ez02n2v0ueryodw/SNuyZEGZhb
FOR YOUR PORTFOLIO
Please see Rhonda Fleischman for any questions.