RECOVER CPR Advanced life support Flashcards
What two monitoring device techniques should be started straight away when performing CPR?
electrocardiogram and end tidal CO2
When should ECG traces be monitored during CPR and why?
During pauses in compressions as it is susceptible to motion artifact
What is end tidal CO2 monitoring useful for?
identification of return of spontaneous circulation
chest compression quality
What are the 3 steps to start advanced life support?
Initiate monitoring (ECG and End Tidal CO2)
Obtain vascular access
Administer reversal agents
When should advanced life support be initiated?
After basic life support (chest compression and ventilation)
Why should alcohol never be used for ECG electrodes during CPR?
Alcohol should NEVER be used as a coupling material during CPR.
Alcohol is highly flammable and may ignite if electrical defibrillation is necessary.
Why should you make sure the ECG monitor is compatible with the electrical defibrillator?
ECG Monitor Compatibility
If using an electrical defibrillator, ensure that either the defibrillator’s ECG monitor is used or that any external ECG unit is safe for defibrillator use.
ECG systems can be damaged by the application of a defibrillator if they are not designed for this use. If you have both a defibrillator and a separate ECG monitor in your practice, contact the manufacturer of the ECG monitor to ensure that it is safe for use with your defibrillator.
Why is it important to carry out uninterrupted cycles when carrying out CPR?
Full 2-minute cycles of chest compressions without interruption are recommended to optimize perfusion to the brain and heart. It takes approximately 1 minute of uninterrupted chest compressions to attain a maximal, steady state blood flow to the heart and other tissues. Prematurely pausing chest compressions prevents development of this maximal, steady state blood flow and results in poor perfusion of the tissues. Chest compressions should never be stopped solely to evaluate the ECG, but instead the ECG should be evaluated during the brief pauses between 2-minute cycles.
Why are ECG signals highly susceptible to artifact?
ECG signals are highly susceptible to artifact due to electrical signals from other equipment in the environment and motion of the patient.
Can ECG readings be evaluated during chest compressions?
While chest compressions are being delivered, the artifact signal is much larger than the ECG signal, and it is generally not possible to accurately interpret the ECG. Attempts to interpret the ECG during chest compressions are likely to lead to erroneous conclusions.
How long should the pause between CPR cycles last?
This pause between cycles should last no more than 2 to 5 seconds and only long enough for a rhythm diagnosis to be made
When should the announcement of the person taking over chest compressions take place?
The recorder or team leader should announce that a change in compressor is about to occur 5 to 10 seconds before the change to allow the new compressor to get into position and to allow any available team members to look at the ECG monitor.
Should a pulse be felt during chest compressions during CPR?
Femoral pulse palpation may be useful during CPR and should be employed if there are enough team members available. Failure to feel a pulse accompanying chest compressions supports a reassessment of technique: and a reconsideration of compression style.
Weak pulses may be appreciated during adequate chest compressions and disappear during compressor rotation
During the pause when the compressor changes, what three major types of rhythms can be seen on the ECG?
The critical diagnostic goal is to determine which of the three major types of rhythms is present: (1) a perfusing rhythm, (2) a non-shockable arrest rhythm, or (3) a shockable arrest rhythm. Only perfusing rhythms are associated with pulses, palpable apex beats, and/or auscultable heart sounds.
How do you detect a perfusing rhythm during CPR?
Perfusing rhythms are repeated rhythms of any shape that generate pulses.
How many non shockable arrest rhythms are there?
There are two non-shockable arrest rhythms, neither of which is associated with effective cardiac output. These are called “non-shockable rhythms” because electrical defibrillation is not effective and may cause additional myocardial injury.
Pulseless electrical activity
Like pulseless electrical activity, asystole is a non-shockable rhythm that should never be defibrillated.
What is pulseless electrical activity characterised by?
Pulseless electrical activity (PEA) is characterized by ECG activity that appears coordinated and repeats at a rate of less than 200 per minute, but is not associated with the generation of a palpable pulse. Most commonly, PEA rhythms have rates of less than 50 per minute and are characterized by narrow QRS complexes. However, PEA can look like a normal sinus rhythm or have wide and bizarre complexes. It is occasionally referred to in older literature as electromechanical dissociation (EMD).
How many shockable arrest rhythms are there?
There are two shockable arrest rhythms, neither of which is associated with effective cardiac output. These are called “shockable rhythms” because electrical defibrillation may be effective and should be done as soon as possible.
pulseless ventricular tachycardia, ventricular fibrillation (VF) is a “shockable” rhythm because electrical defibrillation is the most effective treatment.
What rate would true ventricular tachycradia be?
over 200
What is the major difference between pulse ventricular tachycardia and pulseless electrical activity?
The major differentiating feature between pulseless VT and PEA is the rapid rate
How is pulseless ventricular tachycardia recognised on an ECG?
Pulseless ventricular tachycardia (pulseless VT) is recognized by organized, repeated, wide QRS complexes at a rate greater than 200 per minute without accompanying pulses. The major differentiating feature between pulseless VT and PEA is the rapid rate
How is ventricular fibrillation recognised on an ECG?
VF may be recognized by a wavy chaotic line on the ECG, and may be characterized as either fine ventricular fibrillation (low amplitude, high frequency) or coarse ventricular fibrillation (high amplitude, low frequency). The major differentiating feature of VF is the lack of a consistent, repeated waveform.
Is this statement true or false?
Pulseless electrical activity often has a faster rate than pulseless ventricular tachycardia
FALSE
VF may be recognized by a wavy chaotic line on the ECG, and may be characterized as either fine ventricular fibrillation (low amplitude, high frequency) or coarse ventricular fibrillation (high amplitude, low frequency). The major differentiating feature of VF is the lack of a consistent, repeated waveform.
What does the end tidal CO2 reflect?
The end tidal CO2 (EtCO2) reflects the amount of CO2 in the exhaled air at the end of breath, and is similar to the partial pressure of CO2 in the arterial blood.
What two factors determine the end tidal CO2 factors?
The EtCO2 value will be determined by two main factors: (1) minute ventilation (the product of respiratory rate and tidal volume), and (2) the amount of blood returning from the tissues to the lungs.
Why can the ETCO2 be used to monitor the quality of chest compressions?
Because it is directly related to cardiac output, the EtCO2 can be used to monitor the quality of chest compressions during CPR.
During CPR, the EtCO2 reflects the amount of blood returning from the body to the lungs. EtCO2 will be directly related to the cardiac output. With higher cardiac output, the EtCO2 will be higher, while with lower cardiac output, the EtCO2 will be lower.
What can a sudden increase in ETCO2 indicate (30mmHg)?
Cardiac output increases dramatically upon return of spontaneous circulation ROSC; therefore, a sudden increase in EtCO2 to > 30 mmHg provides a vital clue that ROSC has occurred
What is the only value that can be accurately monitored during chest compressions?
Unlike the ECG, auscultation, direct pulse palpation or echocardiography, the end tidal CO2 can be evaluated while chest compressions are occurring
If there is asudden increase in ETCO2 that may indicate a return of spontaneous circulation what should be done before stopping chest compressions?
In any patient with a sudden increase in EtCO2 during chest compressions, it is important to assess the presence of a pulse before stopping chest compressions. In addition, you can assess for other signs of ROSC, such as voluntary motor movements, chewing on the endotracheal tube, return of the corneal or palpebral reflex, or signs of consciousness. However, until a spontaneous pulse has been definitively identified, chest compressions should be continued.
How can you accurately verify correct ET tube placement during CPR?
Verify accurate ETT placement during CPA using one of the following approaches:
Direct visualization of chest movements during a positive pressure breath
Direct visualization of placement through the arytenoid cartilages during intubation
What are the two main reasons an ETCO2 might read 0 when performing chest compressions?
There are 2 main reasons the EtCO2 may read zero during CPR:
The ETT is in the esophagus
The cuff on the ETT is not sufficiently inflated
How can ventilation affect ETCO2 in CPR?
If ventilation is provided at a rate faster than 10 bpm, or tidal volumes larger than 10 ml/kg are delivered, the EtCO2 will drop. In this case, the decreased end tidal CO2 is due to increased minute ventilation, not lower cardiac output. In order for EtCO2 to be a useful indicator of cardiac output during CPR, breaths must be delivered consistently at a rate of approximately 10 per minute, as described in the basic life support algorithm.
What is PvCO2?
peripheral venous CO2 partial pressure
Can PvCO2 be substituted for EtCO2 during CPR?
PvCO2 (peripheral venous CO2 partial pressure) should not be used as a substitute for EtCO2, as there is often very little association between PvCO2 and EtCO2 during CPA. During CPR, the PvCO2 may be much higher than the EtCO2 because of poor blood flow in the periphery and buildup of CO2 in these peripheral tissues. Using PvCO2 rather than the EtCO2 may lead the rescuer to believe that compression quality is good when, in fact, the EtCO2 may actually be low due to poor blood flow to the lungs
What two main purposes are changes in ETCO2 useful for?
Changes in EtCO2 will reflect changes in blood flow, and are therefore useful for two main purposes during CPR: (1) evaluating the efficacy of chest compressions, and (2) identifying ROSC.
How does compression quality need to be improved if the ETCO2 is below 15 mmHg during CPR?
Compression quality (rate, depth, chest recoil) should be improved during CPR in any patient with EtCO2 values less than 15 mmHg.
How can an improvement in rate, depth and chest recoil be achieved during CPR when the ETCO2 in low?
Increasing compression depth up to one-half the width of the chest
Verifying that the compression rate is between 100 and 120 compressions per minute
Ensuring that compressions are being performed at the correct location on the chest based on the patient’s conformation and size
Taking care not to lean on the chest between compressions to allow for full elastic recoil and filling of the heart
IF chest compressions during CPR are being performed correctly, what elese needs to be assessed if ETCO2 is low?
Remember that increased minute ventilation (respiratory rate greater than 10 per minute and/or large tidal volumes) will decrease EtCO2, even if chest compressions are being done correctly. Therefore, in order to use EtCO2 as a measure of chest compression efficacy, ventilation must be delivered consistently at a rate of 10 breaths per minute, as described in the BLS algorithm.
Other monitoring devices, such as indirect blood pressure monitors and pulse oximeters, are often desirable in emergency and critical care medicine, but during CPR, these devices become less useful.
Why do you think that is?
During CPA, indirect blood pressure monitors and pulse oximeters are not useful due to the lack of adequate pulse pressure.
These devices rely upon pulsatile arterial blood flow that is detectable by the machine, and during CPR, there is typically inadequate pulsatile flow for accurate readings. Attempts to determine either indirect blood pressure or oxygen saturation will result in inaccurate or undetectable results. In addition, like the ECG monitor, both indirect blood pressure monitors and pulse oximeters are highly susceptible to the motion artifact present during chest compressions.
Finally, these monitors may distract resuscitative efforts by providing extraneous or inaccurate information to the team leader.
Which of the following monitoring devices is LEAST likely to be helpful during CPR?
pulse oximeter
capnograph
ECG
Because of motion artifact and lack of a consistent peripheral pulse, the pulse oximeter is unlikely to be of value during CPR. In addition, attempts to get a good signal from a pulse oximeter during CPR can distract team members from more important tasks. On the following screen, watch the video for an example of how focusing on the pulse oximeter can distract the team from doing effective CPR.
IF a central line is not available to use, in what order should peripheral veins be used?
If a patent catheter is available, it should be used. If more than one catheter is present, the catheter closest to the heart should be used in order to improve drug delivery time. A central line will deliver drugs into the venous system closest to the heart and should be used to administer CPR drugs, if available. If only peripheral catheters are available, they should be prioritized in the following order:
Jugular
Cephalic
Saphenous
IF there are several catheters which one should be used for drug delivery during CPR and why?
The catheter closest to the heart should be used in order to improve drug delivery.
dog with veins outlined
In animals without a pre-existing catheter, BLS should begin promptly, and the team leader should provide direction as to the type of vascular access to be obtained. In cases with adequate team members, more than one individual may work on IV catheter placement at separate sites.
How much flush should follow drug administrationin CPR?
Regardless of the location of the catheter, following drug administration the catheter should be flushed with an isotonic crystalloid solution to facilitate flow to the heart and ultimately to the tissues. While there is no specific evidence regarding the volume of flush, in general 3-5 cc in cats, 5-10 cc in small to medium sized dogs, and 10-15 cc in large and giant breed dogs is reasonable.
What are the options for vascular access for drug administration in CPR?
Options for vascular access include:
Percutaneous peripheral venous
Venous cutdown
Intraosseous (IO)
What size catheter can be used for drug administration with CPR?
A smaller than average catheter (e.g., 20-22 G) may be placed more easily than a larger catheter. The initial small-bore catheter can be used during CPR for drug administration. Following ROSC, a larger bore catheter may be placed if needed.
How is an intravenous catheter secured when placed using a cut down?
The catheter is then secured with sutures to avoid dislodgment.
When should intraosseous catheter placement be considered during CPR?
Placement of an intraosseous catheter may be considered when prompt IV access is not practical or possible, or when venous catheterization has been unsuccessful. IO catheters facilitate rapid drug delivery into the central circulation.
What are the common sites for intraosseous catheter placement? What is the preferred site and why?
Many sites are possible for placement of IO catheters. Common sites include the humerus, the femur, and the tibia. Because the humerus is close to the heart, IO catheters in this bone will provide the fastest CPR drug delivery to the sites of action.
Due to the proximity of the humerus to the thorax, where chest compressions are occurring, it is often easier to use the hindlimb during CPR. However, recall that the humerus is closest to the heart, so if it is accessible, it is the preferred site of IO catheter placement.
What size needle can be used for an intraosseous catheter for puppies and kittens?
For kittens and puppies, an 18 or 20 gauge standard needle without a stylet may be used. Alternatively, the use of a spinal needle with stylet will reduce the risk of plugging the needle with bone during placement.
When would intratracheal drug administration be indicated?
In general, IV or IO administration is preferred due to the variable absorption of drugs administered into the trachea. However, intratracheal drug administration may be considered when there is no IV or IO access readily available.
What emergency drugs can be given intratracheal?
Drugs that may be given IT include epinephrine, atropine, and vasopressin.
What emergency drugs should never be given intratracheal?
However, sodium bicarbonate should never be administered IT.
If drugs have been given intratracheal should you stop attempting to get intravenous access?
Recall that IT administration of drugs is a stopgap measure as you continue to attempt to obtain direct vascular access via IV or IO catheterization. As soon as IV or IO access is obtained, drugs should be re-dosed via the IV or IO route.
Is the same amount drug doses given intratracheal compared to other routes?
There is limited experimental evidence to guide IT dosing, but in general, doses of two to ten times IV/IO doses are recommended
how many ml of saline should emergency drugs be diluted with when given intratracheal?
IT drugs should be diluted in 5 to 10 ml of either sterile water or saline.
Why should drugs that are given intratracheal be diluted?
In order for IT drugs to be effective, they must be absorbed across the tracheal/bronchial epithelium and reach the bronchial circulation.
How do you administer drugs intratracheal?
A long catheter, such as a 5 French red rubber catheter, is fed through the endotracheal tube.
The diluted drug is administrated through the red rubber catheter. The syringe delivers a pulse of 5 to 10 ml of air into the red rubber catheter to blow as much of the fluid out of the tube as possible.
The catheter should then be withdrawn from the endotracheal tube and the ventilation bag re-connected. Two breaths should be administered rapidly to help disperse the medication throughout the pulmonary tree.
Which of the following drugs should never be administered IT?
Drugs that may be given IT include epinephrine, atropine, and vasopressin. However, sodium bicarbonate should never be administered IT. Recall that IT administration of drugs is a stopgap measure as you continue to attempt to obtain direct vascular access via IV or IO catheterization. As soon as IV or IO access is obtained, drugs should be re-dosed via the IV or IO route.
Intracardiac administration of emergency drugs is preferred over intratracheal administration.
True or false?
Given the evidence that intratracheal (IT) drug administration leads to therapeutic plasma concentrations of most emergency drugs and the risks associated with blind intracardiac (IC) injections (such as laceration of coronary vessels), the IT route is preferred over the IC route during CPR.
The next card is a summary on access on drug administration
Prompt vascular access is essential to successful outcomes in CPR. Multiple options are available, including percutaneous peripheral catheterization, venous cutdown, and intraosseous catheterization.
If multiple catheters are available, the catheter that is closest to the heart and therefore provides the most rapid delivery of drugs to the central circulation should be used.
If percutaneous catheterization is not immediately successful, a cutdown procedure may be performed to achieve venous access.
Rapid vascular access may be obtained using intraosseous (IO) catheters as well.
If venous or IO catheterization is not possible, certain drugs may be administered intratracheally. In this scenario, attempts at IV or IO catheterization should continue and drugs re-dosed as soon as vascular access is achieved.
Why do you think it is important to administer reversal agents intravenously?
Reversal Agents for Sedatives: Intravenous Drug Delivery
Intramuscular or subcutaneous administration of reversal agents is not recommended in patients with CPA due to slow, unpredictable uptake. Therefore, intravenous or intraosseous administration of reversal agents is recommended in patients with CPA.
You sedated a dog to repair a laceration with hydromorphone and dexmedetomidine. After the dog was placed in a cage, he is found in CPA.
Because the drugs were administered over 1 hour ago, there is no reason to administer the reversals.
True or False?
In general, if a reversible sedative or anesthetic agent has been administered to an animal with CPA, early intravenous treatment with a reversal agent is indicated. Even if the drug was administered several hours before the CPA occurred, reversal is generally safe and may still have some positive effects.
A patient with a GDV presents to your clinic. You sedate with hydromorphone and trocharize the stomach to stabilize him. You are reassessing him after trocharization and he begins taking agonal breaths and then stops breathing. After initiating basic life support, your next step is to administer naloxone to reverse the hydromorphone.
True or False?
Remember from the RECOVER CPR algorithm that the first step in initiating Advanced Life Support is to connect the ECG and EtCO2 monitors. Next we should verify that our vascular access is present and patent. Only after those 2 steps are completed should reversal agents be administered. Reversal agents do not directly treat CPA, but are adjunctive therapies that may improve the chances of achieving ROSC. Always remember to follow the steps of the algorithm in order.
For patients in CPA, IV fluid therapy should be reserved only for those patients with documented or suspected hypovolemia.
Why do you think that is?
IV fluid therapy is helpful for improving cardiac output in patients with documented or suspected hypovolemia, but may be detrimental in euvolemic patients with CPA due to reduced blood flow and oxygen delivery to core organs.
What is the amount of blood flow and oxygen delivered to a tissue bed determined by?
The amount of blood flow, and hence oxygen delivered, to a tissue bed is determined by the force driving blood into the tissue bed, the resistance to flow offered by the vasculature in the tissue bed, and the force pushing back at the outflow of the tissue bed
What is the driving force for blood flow to most tissue?
The driving force for blood flow to most tissues is the mean arterial blood pressure (MAP), and the outflow force pushing back is the central venous blood pressure (CVP)
How does intravenous fluids help in a patient that is hypovolaemic with spontaneous circulation?
In hypovolemic patients with spontaneous circulation, IV fluid therapy can improve cardiac output and increase MAP because of the relationship between stretch of the ventricles and the subsequent ability of the ventricle to contract more fully due to that stretch. With increased intravascular volume provided by IV fluid therapy, the ventricles experience greater stretch and hence can contract more and increase cardiac output.
Explain how intravenous fluid therapy can be detrimental in patient in cardiopulmonary arrest that is euvolaemic?
If a patient in CPA is euvolemic and fluids are administered intravenously, it is unlikely that cardiac output will increase significantly because the ventricles are not spontaneously contracting. Therefore, fluids administered IV will accumulate in the venous circuit, which is more distensible than the arterial circuit, resulting in increased central venous pressure (CVP) rather than increased MAP. This increase in CVP leads to higher pressure on the outflow side of the tissue bed, resulting in decreased blood flow and oxygen delivery to the tissues. Therefore, in patients in CPA that are euvolemic, fluids should be administered conservatively if at all, until ROSC is achieved and the heart is again contracting spontaneously.
How does intravenous fluids help with hypovolaemia in patients in cardiopulmonary arrest?
For patients in CPA with known or suspected hypovolemia, boluses of IV fluids may be beneficial to provide additional circulating volume. Although CVP will increase, the increased stretch of the ventricles will lead to improved cardiac output, increasing MAP and improving blood flow to the tissues. Patients with trauma, severe vomiting and/or diarrhea, or hemorrhage are likely to benefit from fluids.
Can glucocorticoids be used in patients with cardio pulmonary arrest?
Potentially Detrimental Side Effects of Glucocorticoids
There is a growing body of evidence that corticosteroids may have detrimental effects in many cases, and given the weak evidence supporting their use, glucocorticoids should be avoided unless there is a clear indication. Glucocorticoids have many potentially detrimental side effects that may be particularly dangerous in patients with CPA. Because they are counter-regulatory hormones in glucose metabolism, glucocorticoids commonly cause hyperglycemia, which can perpetuate brain injury in patients with brain ischemia, common in CPA. Glucocorticoids also very commonly lead to gastrointestinal ulceration in dogs, causing significant blood loss and/or bacterial translocation leading to septicemia. In both dogs and cats, they decrease prostaglandin production in the kidney, compromising renal perfusion and potentially leading to ischemic acute kidney injury.
What patients may benefit from glucocorticoid administration in cardiopulmonary arrest?
Patients That May Benefit from Glucocorticoids
However, glucocorticoids may be warranted in certain patient populations. For instance, animals that arrest in association with anaphylactic shock may benefit from anti-inflammatory doses of glucocorticoids (0.1 mg/kg dexamethasone SP IV). Patients with concurrent hypoadrenocorticism (i.e., Addison’s disease) will also benefit from glucocorticoids. Finally, animals that develop critical illness-related corticosteroid insufficiency (CIRCI) after ROSC may also benefit from physiologic steroid therapy. Corticosteroids should only be used during CPR if the patient is known to have or is highly suspected of having one of these disorders. For the vast majority of patients, corticosteroids should not be administered during CPR.
What are the potential benefits of open chest cardiopulmonary resuscitation?
Potential benefits of open-chest CPR (OCCPR):
Better cardiac output
Higher rates of ROSC
Direct assessment of the heart
What may be some of the specific indications for open chest CPR?
Specific indications for OCCPR include:
Pleural space disease such as large volume pleural effusion or pneumothorax
Pericardial effusion
Patients already under anesthesia for thoracic or abdominal surgery
Giant breed dogs with round chest conformations, such as Mastiffs, Saint Bernards, and some Great Danes
What needs to be carried out to perform an open chest CPR?
OCCPR requires:
A rapid emergency thoracotomy for direct cardiac massage
Closure of the thorax
Post-cardiac arrest care
Why is pleural space disease an indication for open chest CPR?
Pleural space disease, such as large volume pleural effusion or pneumothorax, is an indication for OCCPR. Because of the markedly increased intrathoracic pressure in patients with severe pleural space disease, venous return to the heart is compromised and external chest compressions are unlikely to result in forward flow out of the heart. Opening the chest relieves the pressure exerted by the pleural space disease and allows the heart to fill so that chest compressions are effective.
Why is pericardial effusion an indication for open chest CPR?
Pericardial effusion is an indication for OCCPR because cardiac tamponade impedes return of blood to the atria, resulting in minimal cardiac output during external chest compressions. OCCPR allows the rescuer to open the pericardium and remove the pericardial effusion.
Why is thoracic or abdominal surgery an indication for open chest CPR?
OCCPR should be initiated in patients under anesthesia for thoracic or abdominal surgery. For patients undergoing thoracotomy, easy access to the heart for direct cardiac compressions is already available. For patients having abdominal surgery, rolling them into lateral recumbency for chest compressions is not feasible, and direct cardiac compressions can easily be achieved by incising through the diaphragm and compressing the heart through the diaphragmatic incision.
Why is round chest comformations in dogs an indication for open chest CPR?
Giant breed dogs with round chest conformations
In giant breed dogs with round chest conformations, OCCPR is more likely to be of benefit than closed-chest CPR. This is because they have poorly compliant chests that are difficult to compress adequately to generate enough intrathoracic pressure to provide substantial blood flow using the thoracic pump approach.
On the other hand, in cats or in small dogs (<10 kg), in which external chest compressions are more effective due to higher chest compliance, OCCPR is not indicated; in these animals, internal cardiac massage is more challenging due to the small size of their thoracic cavities.
You’re seeing a Gordon Setter with a large volume pyothorax. The owner has authorized any life-saving treatment you feel is in the dog’s best interest.
The dog develops CPA during IV catheter placement. What should you do?
immediate open chest CPR? or close chested CPR?
If OCCPR is to be pursued, it is best to begin the procedure as early in the course of a resuscitative effort as possible. This is why it is important to obtain a CPR code (red, yellow, or green) in any patient admitted to the hospital as discussed in the BLS course. In this case, because the dog has pleural space disease, OCCPR should be pursued.
What is the first step of advanced life support?
ECG
ECG monitoring is an essential part of ALS. The ECG rhythm diagnosis is the primary decision point in the ALS portion of the CPR algorithm. It is therefore important that attachment of ECG leads be a priority after BLS has been started.
Tom presented on emergency for lethargy.
On physical exam, he had pale oral mucous membranes, poor pulse quality, and was assessed to be 8-10% dehydrated. Additionally, he had a large firm bladder. Immediately following palpation of the bladder, Tom screamed and collapsed in CPA.
What is your first step?
start one-handed compressions, intubate and ventilate
While Tom is likely suffering from a urethral obstruction, CPA requires immediate support of the cardiovascular system. Additionally, while intravenous fluids will likely be useful in this case, the first priority must be restoration of circulation via chest compressions in the patient with CPA. Finally, while determining the arrest rhythm will help guide ALS therapy, the first priority in any patient in CPA is initiation of BLS.
Now that you have started BLS, which of the following monitoring devices would be high priorities?
ECG
While indirect blood pressure monitors and pulse oximeters are often desirable in emergency and critical care medicine, during CPR, these devices become less useful due to the lack of adequate pulse pressure. These devices rely upon pulsatile arterial blood flow, and during CPR, adequate pulsatile flow for device function is typically absent. Attempts to determine either indirect blood pressure or oxygen saturation will result in inaccurate or undetectable results. Equally importantly, attempts to use these monitors may distract the people available for assisting in resuscitative efforts, and provide extraneous and inaccurate recommendations for the team leader.
In placing an IV catheter in Tom (a cat), what is your top priority in cardiopulmonary arrest?
Prompt vascular access is essential for increasing the likelihood of a successful outcome of CPR. Immediate venous cutdown or placement of an IO catheter should be considered when prompt percutaneous access is not practical or possible, or when venous catheterization has been unsuccessful.
Tom’s (a cat) owner is insistent upon the best possible outcome and asks you to perform open-chest CPR. How would you respond?
Explain that open chest CPR is not warranted in cats
Open-chest CPR (OCCPR) has only been associated with a higher rate of ROSC than closed-chest CPR in experimental studies in dogs with VF. It is unlikely to be of benefit over closed-chest CPR in cats or in small dogs (<20 kg) because these smaller animals have greater chest compliance and the thoracic cavity is very small, making internal chest compressions very difficult.
What would be a reasonable initial IV fluid plan for Tom (a cat) during CPR? 8-10% dehydrated
Tom’s initial physical exam was consistent with hypovolemic shock (pale mucous membranes, prolonged CRT, poor pulse quality) and he would likely benefit from an initial fluid bolus. 20-30 ml/kg represents 1/3-1/2 of his total blood volume (60 ml/kg in a cat) and would be a reasonable fluid bolus in this case. 90 ml/kg is an excessive amount for an initial bolus, and a fluid rate of 2 ml/kg is unlikely to address his hypovolemia rapidly enough. If Tom had been euvolemic, withholding fluids during CPR would have been most appropriate, but given the evidence of hypovolemia, a 20-30 ml/kg bolus over 15 minutes is the best choice.
Ruby has been progressively lethargic and anorexic for several days. On initial examination, she is weak with bounding pulses and icterus. An IV catheter is placed and point-of-care blood work shows that she has a hematocrit of 14%, total solids of 7.2 gm/dl, icteric serum and autoagglutination. As you are finishing placing an IV catheter, Ruby vomits and collapses in cardiopulmonary arrest. What is your first step?
Start chest compressions, intubate and ventilate
While Ruby is likely suffering from an immune-mediated hemolytic anemia, CPA requires immediate support of the cardiovascular system. While steroids, blood products, and a fluid bolus may all be part of her initial therapy, the first priority in any patient in CPA is initiation of BLS.
Explaijn what pulseless electrical activity would look like on a ECG monitor?
There are consistent, repeated QRS complexes that are narrow at a rate of less than 200 per minute with no associated pulses, so this is most likely pulseless electrical activity. Had the rate been greater than 200 per minute with wide complexes, pulseless VT would have been more likely.
According to the RECOVER CPR algorithm, which of the following would be the first step in initiating advanced life support in a patient with a patent intravenous catheter in place that arrested due to an inadvertent overdose of hydromorphone?
attach ecg leads
During CPR, what is the minimum EtCO2 associated with good quality chest compressions?
15 mm Hg
Which of the following is the best choice to improve contact between an ECG alligator clip and a patient’s skin during CPR?
Electrode gel
A patient arrests during induction for a spay surgery. After the first cycle of BLS, you diagnose asystole and decide to administer epinephrine. Which of the following would be the best route of administration?
Cephalic intravenous catheter
Via a red rubber catheter through the endotracheal tube
Intracardiac injection
Lateral saphenous intravenous catheter
Cephalic intravenous catheter
A patient was premedicated for an enucleation and spay with dexmedetomidine and methadone. Surgery was complicated and took 3 hours. One hour after extubation, the patient experienced CPA. Which of the following statements is true?
Because it has been 4 hours since administration of the premedication, reversal agents are unlikely to be effective
Flumazenil and naloxone are indicated
Atipamezole and naloxone are indicated
Atipamezole and flumazenil are indicated
Atipamezole and naloxone are indicated
The ECG is the most useful monitoring device for diagnosing a return of spontaneous circulation during CPR. true or false?
false
Because there is stronger evidence of harm than of benefit in patients with CPA, the use of corticosteroids during CPR is not recommended. true or false?
true
Which is the preferred approach for open-chest CPR in most patients?
Left lateral thoracotomy (right lateral recumbency)
Right lateral thoracotomy (left lateral recumbency)
Median sternotomy (dorsal recumbency)
Right lateral thoracotomy (left lateral recumbency)
You admit a 40kg greyhound to the hospital for a GI foreign body surgery. When discussing the option of open-chest CPR, the owner asks if it would be reasonable to try closed-chest CPR and convert to open-chest CPR if initial attempts are unsuccessful. Which of the following is the correct response to that question?
Because of the morbidity associated with open-chest CPR, it is reasonable to start with closed-chest CPR and convert to open-chest if there is no response
Because her dog is keel-chested, better cardiac output can be achieved with closed-chest CPR than with open-chest CPR
Her dog is more likely to have a good outcome with immediate open-chest CPR than with closed-chest CPR
Her dog is more likely to have a good outcome with immediate open-chest CPR than with closed-chest CPR
In euvolemic patients in cardiopulmonary arrest, a fluid bolus should be given as soon as possible after CPR is initiated to improve perfusion to the core organs.
false
Are shockable rhythms common in dogs and cats?
Remember that non-shockable rhythms are the most common arrest rhythms in dogs and cats.
What 3 different types of rhythms are you focusing on when looking at the ECG
ECG analysis during CPR is focused on differentiating three major types of arrest rhythms:
Perfusing rhythms associated with pulses
Non-shockable arrest rhythms that do not require electrical defibrillation
Shockable arrest rhythms that require electrical defibrillation
When should the ECG be reviewed?.
During the brief pause in compressions between cycles of BLS, the team leader should interpret the ECG and announce the rhythm diagnosis. Agreement should be reached among all team members as to the ECG rhythm diagnosis; if consensus is not reached immediately, chest compressions should be re-started and the discussion about rhythm diagnosis can continue during the next cycle of compressions. Ultimately, if consensus cannot be reached, the team leader should make the diagnosis after considering input from all team members. Chest compressions should never be stopped during a cycle of BLS strictly to evaluate the ECG. However, if there is a sudden rise in EtCO2, and a strong, palpable pulse is noted during a cycle of BLS, it is reasonable to briefly pause chest compressions to review the ECG and palpate the pulse to determine if ROSC has truly been achieved.
What should you do if there are repeated complexes and a palpable pulse? What does this mean?
If repeated complexes are present, quickly palpate the pulse or apex beat to determine if there is blood flow associated with the complexes.
If there are pulses, this is a perfusing rhythm and the patient has achieved a return of spontaneous circulation, so chest compressions can be discontinued.
How long should pulse assessment take? What should you do if you have doubt there is a pulse?
Pulse assessment should take no more than five seconds. If there is any doubt as to whether a pulse is present, assume that one is not present and continue BLS.
If a patient receiving CPR has repeated ECG complexes on the ECG but no palpable pulse and a HR of less than 200 what is this called?
A rate of less than 200 per minute is most consistent with pulseless electrical activity (PEA), a non-shockable rhythm.
In this case, the PEA/Asystole ALS algorithm should be followed. We will discuss treatment of PEA/Asystole in detail later in the module.
Is pulseless electrical activity shockable or not?
not shockable
If a patient receiving CPR has repeated ECG complexes on the ECG but no palpable pulse and a HR over 200 what is this called?
pulseless ventricular tachycardia
Is ventricular tachycardia shockable or not?
shockable
If a patient receiving CPR has repeated ECG complexes and palpable pulses, what is this called?
a perfusing rhythm
If a patient receiving CPR does not have repeated ECG complexes and the ECG is flat lined? What is this called?
Asystole
is asystole shockable?
not shockable
If a patient receiving CPR does not have repeated ECG complexes but the ECG is not flat lined? What is this called?
ventricular fibrillation
What is typically the rate for pulseless electrical activity?
Typically, the rate for PEA is much lower (less than 50 per minute)
What is happening with the electrical conduction system and ECG waveform in pulseless electrical activity?
Recall that with PEA, the electrical conduction system of the heart is active and generates a measureable ECG waveform, but there is no mechanical activity in the heart and no blood flow out of the heart.
What is happening to the heart in pulseless ventricular tachycardia?
Recall that with pulseless VT, the ventricles are contracting, but the heart rate is so fast that there is no time for the ventricles to fill and thus no significant flow of blood out of the heart
How does the ECG complexes differ between pulseless electrical activity and ventricular tachycardia?
The following is an example of pulseless VT. Note that in this example, the rate is 236 per minute. Also note that the QRS complexes are wider than the PEA example. Although the rate is the most reliable feature differentiating PEA from pulseless VT, the QRS complexes are also usually relatively wider in pulseless VT than in PEA
What electrical and mechanical activity occurs with ventricular fibrillation?
Recall that animals with ventricular fibrillation have random electrical and mechanical activity within the ventricles, causing them to quiver, but not to generate blood flow out of the heart.
Are there consistent, repeating complexes? YES
Are pulses associated with the complexes? NO
Is the rate > 200/min? NO
What is the diagnosis?
pulseless electrical activity
Are there consistent, repeating complexes? YES
Are pulses associated with the complexes? NO
Is the rate > 200/min? YES
What is the diagnosis?
Pulseless ventricular tachycardia
Are there consistent, repeating complexes? YES
Are pulses associated with the complexes? YES
What is the diagnosis?
Diagnosis = Perfusing Rhythm/ROSC
Are there consistent, repeating complexes? NO
Is the ECG a flat line? YES
What is the diagnosis?
Asystole
Are there consistent, repeating complexes? NO
Is the ECG a flat line? NO
What is the diagnosis?
Ventricular fibrillation
What does the electrical defibrillation do?
ALS therapy also targets the shockable rhythms (VF and pulseless VT) by stopping the uncoordinated or excessively rapid ventricular activity using electrical or mechanical defibrillation
How can you differentiate between pulseless ventricular tachycardia and perfusing ventricular tachycardia?
These rhythms can only be differentiated by palpating a pulse. Although there may be some pulse deficits, perfusing VT will be associated with a pulse or apex beat for most ECG complexes, while patients in pulseless VT will not have pulses associated with any complexes. Additionally, animals with pulseless VT will be collapsed and unresponsive, while animals with perfusing VT will be conscious, although they may appear weak or pale.
What are the two categories of perfusing tachycardia?
Two Categories of Perfusing VT
There are two categories of perfusing VT: stable VT (also called an accelerated idioventricular rhythm, or AIVR) and unstable VT
What causes perfusing ventricular tachycardia?
Both indicate underlying ventricular myocardial ischemia or disease, causing groups of myocardial cells to drive the heart rhythm rather than the SA node, as the myocardial cells are depolarizing at a rate faster than the SA node. Most commonly, these rhythms occur in dogs due to systemic diseases that affect myocardial perfusion, but occasionally they may occur because of intrinsic cardiac disease.
What is stable ventricular tachycardia also known as?
Stable VT is also called an accelerated idioventricular rhythm (AIVR)
What happens physiologically when a patient has stable ventricular tachycardia? What would the heart rate usually be?
It is a ventricular arrhythmia that generates blood flow sufficient for oxygen delivery to the tissues of the body, and hence the patient has a normal blood pressure. It generally results in a heart rate of less than 180 beats per minute and often alternates with a sinus rhythm.
Does stable tachycardia require treatment?
In many patients, this rhythm will require no direct therapy, but if the complexes are of varying shapes and sizes (multiform ventricular premature contractions), there may be widespread myocardial ischemia or injury, and therapy may be warranted, as the patient may be at increased risk of degenerating into unstable VT or ventricular fibrillation.
Describe the pathophysiology of unstable ventricular tachycardia?
Unstable VT is a ventricular tachyarrhythmia that generates insufficient blood flow and results in arterial hypotension (mean arterial blood pressure <80 mmHg). It may occur at any rate, but typically in dogs it results in a heart rate greater than 180 beats per minute.
How might the ECG appear with unstable ventricular tachycardia?
Unstable VT may also include runs of the R on T phenomenon, where the flat baseline of the ECG disappears and the ECG takes on a “sine wave” appearance
What might unstable ventricular tachycardia be caused by?
Unstable VT may occur due to systemic disease resulting in myocardial ischemia, and may also reflect underlying cardiac disease.
Would you treat unstable ventricular tachycardia?
In most cases, it should be treated with antiarrhythmic drugs.
What drugs can be used to treat unstable ventricular tachycardia?
Options for treating unstable VT or very rapid (>180 bpm) stable VT include lidocaine (2 mg/kg slow IV over 1–2 minutes; may be repeated up to three times), amiodarone (0.5 mg/kg diluted 1:10 with D5W slow IV over 1–2 minutes), or procainamide (2–6 mg/kg slow IV over 1–2 minutes). Amiodarone can cause allergic reactions in dogs, so when using it to treat VT, it is important to monitor closely for signs. All three drugs can slow the rate of ventricular myocardial cells.
What dose of lidocaine can be used to treat unstable ventricular tachycardia? how often can this be used?
lidocaine (2 mg/kg slow IV over 1–2 minutes; may be repeated up to three times)
What is the most common catecholamine used during CPR?
This is a vasopressor - The catecholamine used most commonly during CPR is epinephrine, although other catecholamines such as norepinephrine, methoxamine, and phenylephrine have also been used.
What do catecholamines do to peripheral vessels?
Catecholamines cause peripheral vasoconstriction via peripheral α-1 adrenergic receptors. Epinephrine also stimulates other adrenergic receptors, such as β-1 and β-2 receptors, but these effects are unlikely to be beneficial during CPR and may, in fact, be harmful.
Which drug is most superior to use in CPR, catecholamines or arginine vasopressin?
AVP (or simply vasopressin) acts independently of the adrenergic receptors via peripheral V1 receptors. Therefore, it does not have any of the negative effects caused by stimulation of the other adrenergic receptors. Epinephrine also stimulates other adrenergic receptors, such as β-1 and β-2 receptors, but these effects are unlikely to be beneficial during CPR and may, in fact, be harmful.
What three options are there for vasopressor therapy during CPR?
There are three options for vasopressor therapy use during CPR: low-dose epinephrine, high-dose epinephrine, and vasopressin.
What is the dose for low dose epinephrine during CPR?
Low-dose epinephrine (0.01 mg/kg)
What is the vasopressin dose for first choice therapy in CPR?
vasopressin (0.8 units/kg)
What is the dose for high dose epinephrine?
High-dose epinephrine (0.1 mg/kg)
When should high dose epinephrine be used in CPR and why?
High-dose epinephrine (0.1 mg/kg) has been associated with substantial negative side effects and should only be considered if CPR is prolonged (>10 minutes) and as a last attempt, when CPR is becoming futile
What dose of epinephrine is advised in a patient receiving CPR that has good blood flow (ETCO2 15mmHg) after 10 minutes?
In patients with acute, reversible disease in which good blood flow is being achieved (EtCO2 > 15 mmHg), continuing low-dose epinephrine even after 10 minutes of CPR is the best option. High-dose epinephrine should only be used as a last attempt in a patient in whom you feel CPR is likely becoming futile. This is why the high-dose epinephrine line is printed in light grey on the RECOVER drug and dosing chart shown below.
What route of administration can vasopressors be given?
Vasopressors may be administered IV, IO or IT. Recall that the catheter closest to the heart should be used for intravascular drug therapy to expedite distribution to the sites of action.
What is epinephrine also referred to as?
Outside of the U.S., epinephrine is referred to as adrenaline.
Where is epinephrine naturally produced in the body?
It is naturally produced in the adrenal medulla
What adrenergic receptors does epinephrine stimulate?
Epinephrine stimulates α-1, β-1 and β-2 adrenergic receptors
Aside from peripheral vasoconstriction what effects does epinephrine have on the body?
its physiologic roles are associated with the “fight or flight” response, including peripheral vasoconstriction, increased heart rate, increased cardiac contractility, and bronchodilation.
Which dose of epinephrine is associated with a higher rate of return of spontaneous circulation?
While it is associated with a higher rate of ROSC, it is also associated with worse neurological function in survivors and reduced hospital discharge rates.
What strength is epinephrine usually supplied at?
Epinephrine is supplied at 1 mg/ml,
What type of rhythms should epinephrine be used for in CPR?
Low-dose epinephrine should be used initially for treatment of all non-shockable arrest rhythms
How often should epinephrine be repeated in CPR?
It may be repeated every 3-5 minutes during CPR (or every other cycle of BLS).
Should epinephrine be administered to patients with acute reversible disease after 10 minutes of CPR and why?
In patients with acute, reversible disease, it is recommended that low-dose epinephrine be administered even after 10 minutes of CPR to maximize the chance of survival to discharge.
What negative impacts are high dose of epinephrine associated with and what is the negative impact caused by?
it is also associated with worse neurological function in survivors and reduced hospital discharge rates. It is believed that this negative impact is due to extreme vasoconstriction leading to more severe peripheral acidosis from poor perfusion and from increased myocardial oxygen demand during the post-cardiac arrest period. The β-1 effects of increased cardiac contractility and increased heart rate are likely to blame
What effect does acidaemia have on epinephrine?
The Effect of Acidemia
–
Epinephrine is most effective at physiological pH values and is progressively less effective as acidemia develops. Patients with CPA commonly develop metabolic acidosis from accumulation of lactate and uremic toxins from poor perfusion, as well as respiratory acidosis from hypoventilation and poor peripheral perfusion. Therefore, the vasoconstrictive effects of epinephrine may be blunted during CPR, and the use of an alternate vasopressor such as vasopressin may be warranted, especially in patients with prolonged CPA.
Why would a patient in cardiopulomary arrest be acidaemic?
Patients with CPA commonly develop metabolic acidosis from accumulation of lactate and uremic toxins from poor perfusion, as well as respiratory acidosis from hypoventilation and poor peripheral perfusion
Aside from epinephrine being a β-1 stimulator what other effect does it have?
Via β-1 stimulation, epinephrine is also a positive inotrope and chronotrope, although this is not its primary indication in CPR. Following ROSC, this positive inotropy and chronotropy may increase myocardial oxygen demand, potentially worsening myocardial ischemia, and may lead to tachyarrhythmias. The use of high-dose epinephrine may worsen these undesirable effects.
What effect does epinephrine have on myocardial oxygen demand?
epinephrine is also a positive inotrope and chronotrope, although this is not its primary indication in CPR. Following ROSC, this positive inotropy and chronotropy may increase myocardial oxygen demand, potentially worsening myocardial ischemia, and may lead to tachyarrhythmias.
What type of arrest rhythm should vasopressin be used for?
Vasopressin is an alternative vasopressor that can be used to treat non-shockable arrest rhythms.
What effects does vasopressin have on the body?
Vasopressin (also referred to as arginine vasopressin) is a hormone primarily involved in total body water balance via stimulation of V2 receptors in the renal collecting ducts. In addition to its effects on water balance via V2 receptor stimulation, vasopressin also stimulates V1 receptors on the peripheral vasculature and is a potent vasopressor when given at supraphysiological doses. This is the drug’s primary use during CPR.
What strength is vasopressin usually supplied at ?
Vasopressin is supplied as a 20 U/ml solution
How often can vasopressin be given?
it may be repeated every 3-5 minutes during CPR (or every other cycle of BLS).
What is the dose for vasopressin and what is the administration route during CPR?
dosed at 0.8 U/kg IV/IO or 4–8 U/kg IT during CP
What is the preferred vasopressor to use during CPR with acidaemia and why?
Vasopressin may potentially be preferable to epinephrine in some patients because V1 receptor responsiveness is not affected by pH. Therefore, the drug is more likely to be efficacious in patients with respiratory and metabolic acidoses, which commonly occur with prolonged CPA.
During the first ten minutes of CPR on a patient with asystole, which of the following vasopressor treatment strategies would be appropriate?
- high dose epinephrine every other BLS cycle
- phenylephrine every third cycle of BLS
- vasopressin every BLS cycle
- low dose epinephrine every other BLS cycle
Vasopressor therapy, either low-dose epinephrine, vasopressin, or both, should be administered once every two cycles of BLS, or every 3–5 minutes during CPR, to treat asystole or PEA. High-dose epinephrine is recommended only with prolonged CPR (>10 minutes), and should be considered a “last ditch attempt” to obtain ROSC with the understanding that it may have a negative impact on overall outcome. Administering a vasopressor every cycle of CPR leads to excessive vasoconstriction.
What disease processes are a high vagal tone associated with?
High vagal tone may occur with:
Severe gastrointestinal disturbances (vomiting, diarrhea)
Diseases of the respiratory tract (coughing)
Ophthalmologic surgery
Laryngeal manipulation, such as intubation
Opioid analgesic administration
What may stimulation of the vagus nerve lead to?
High parasympathetic tone to the heart via stimulation of the vagus nerve may lead to severe bradycardia and cardiac arrest. It can be caused by a number of disease processes and therapies.
What may bradycardia causes by a high vagal tone be described as on an ECG?
Effects of High Vagal Tone
High vagal tone causes bradycardia, and may be appreciated on an ECG as sinus bradycardia, AV block, or a pronounced sinus arrhythmia
What can a decrease heart rate caused by a high vagal tone lead to?
This decrease in heart rate can lead to low blood pressure, decreased perfusion to the heart, and, ultimately, cardiac arrest.
What drugs can be used for patients with vagally mediated bradycardia?
The Use of Parasympatholytics
In critically ill patients where CPA is considered imminent, parasympatholytics may prevent or treat vagally-mediated bradycardia. Prevention or treatment of bradycardia may be adequate to prevent CPA
How can parasympathetic drugs help in cardiopulmonary arrest?
For animals in CPA, parasympatholytics are often used to eliminate vagal tone, which may remove the inhibitory stimulation of the vagus nerve on the heart during CPR and increase heart rate following ROSC.
What are the most commonly used parasympathetic drug that is used during CPR?
Atropine is the most commonly used parasympatholytic during CPR. Glycopyrrolate may also be used, but is less commonly chosen because it is less potent and longer acting, making it more difficult to titrate the dose in acute cases.
What effect does Atropine have on the heart?
Atropine is a parasympatholytic drug that is widely used in veterinary medicine.
IV atropine will have a brief paradoxical effect of slowing the heart rate by acting on central muscarinic receptors and causing a transient increase in vagal tone. This effect is rapidly overcome by elimination of vagal tone peripherally, leading to increased heart rate.
What dose of atropine is most commonly used during CPR?
Atropine is most commonly given during CPR at a dose of 0.04 mg/kg in order to increase the heart rate
How often should atropine be administered and how many times?
However, due to its longer half life, this drug should only be repeated once during a CPR attempt. It may be given either at the same time as vasopressors or on alternate cycles.
What administration route should atropine be given?
Atropine may be administered IV, IO, or IT, and as with all arrest drugs, should be administered through the catheter located closest to the heart.
If atropine is administered intratracheal then how should drug preparation be changed?
If administered IT, the dose should be doubled and the drug diluted with sterile saline or water. A red rubber catheter should be passed through the ET tube and Atropine administered through the red rubber catheter, followed by an air flush.
What other effects might atropine have aside from increasing heart rate?
Atropine causes the pupils to dilate and may block the pupillary light reflex, so evaluation of the pupil size and responsiveness may not be useful for assessing neurologic status in patients that have been treated with atropine during CPR. Additionally, ROSC will generally precede the return of the corneal reflex.
During enucleation surgery in a kitten, the heart rate is noted to be 100 bpm. Sudden, severe bradycardia (HR <40) develops and is immediately followed by asystole. After turning off the inhalant, what is the correct CPR sequence?
In cases of bradycardic arrests mediated by high vagal tone, atropine is likely to be of benefit and should be administered as soon as possible during CPR. However, the first step once CPA has been diagnosed is to begin basic life support. In addition, even in a vagally mediated bradycardic arrest, initial drug therapy should prioritize a vasopressor, as there is more evidence supporting a beneficial effect for vasopressors than for parasympatholytic drugs during CPR.
What blood PH level does catecholamines have the best effect?
Acidosis limits the efficacy of catecholamines, which have the greatest effect at a normal pH of 7.4.
Why does acidosis occur in CPR patients and what PH level is blood most commonly at?
Acidosis resulting from lactate and CO2 accumulation may become severe during CPA, and pH of <7.0 is commondosis resulting from lactate and CO2 accumulation may become severe during CPA, and pH of <7.0 is common
How can CPR affect calcium levels?
Hypocalcemia commonly develops during prolonged CPA. Because calcium is essential for skeletal and smooth muscle function, hypocalcemia can have detrimental effects on cardiac function and vascular tone.
How does CPR affect the myocardium?
Myocardial Ischemia
Due to decreased blood flow, myocardial ischemia and necrosis can develop with prolonged CPA. Achieving ROSC is more difficult when the myocardium becomes ischemic, and the heart becomes resistant to defibrillation if VF or pulseless VT develops, making survival less likely.
When is CPR considered prolonged?
Asystole and PEA are considered prolonged after 10 minutes. Often, it is impossible to know the duration of CPA if the initial CPA was unobserved. In the case of an unwitnessed arrest, consider the arrest time to be the time CPR was initiated.
What is bicarbonate therapy in CPR?
Sodium bicarbonate is a potent alkalizing agent,
What negative effects can bicarbonate therapy have on a patient receiving CPR?
However, administration of sodium bicarbonate can result in an increase in serum osmolarity, alkalemia, and potentially a paradoxical cerebral and metabolic acidosis.
At what stage of CPR would bicarbonate therapy be considered?
Therefore, it should be reserved for use only in cases of prolonged CPA, and preferably in animals in which severe metabolic acidosis has been explicitly diagnosed by blood gas analysis.
What effect may bicarbonate therapy have on epinephrine?
α-1 receptors are more responsive to catecholamines at a physiological pH (near 7.40). In cases of prolonged CPA with documented metabolic acidosis, sodium bicarbonate therapy may be useful to maximize the effectiveness of epinephrine.
What negative impacts may excessive bicarbonate therapy have on dogs receiving CPR?
Excessive bicarbonate therapy during CPR in dogs has been associated with pH values of up to 7.8 and dissociation between arterial and CSF pH that might contribute to post-CPR cerebral depression
When is sodium bicarbonate therapy in CPR warranted?
Therefore, judicious use of sodium bicarbonate, preferably only after documentation of severe metabolic acidosis (pH less than 7.0) with blood gas analysis, is warranted.
What is the dose for bicarbonate therapy?
Bicarbonate may be administered at 1 mEq/kg IV or IO if you document a pH < 7.0. It should not be administered IT because it is not effective and can lead to pulmonary irritation
What treatment is given if hyperkalaemia is present during CPR?
If hyperkalemia is documented during CPR, treatment with 10% calcium gluconate IV (0.5 mL/kg) is recommended. This therapy normalizes the difference between resting membrane potential and threshold potential in cardiac cells.
What treatment is given if hypocalcaemia is present during CPR?
If hypocalcemia is documented during CPR, administration of 10% calcium gluconate IV (0.5 mL/kg) is reasonable to improve cardiac contractility and vascular tone.
Lexi: Post-operative Septic Peritonitis
Lexi has been recovering from surgery for septic peritonitis due to an intestinal perforation from a foreign body. She has been given isotonic crystalloid fluids at 150 ml/hr, fentanyl at 3 µg/kg/hr, and broad spectrum antibiotics.
Over the last few hours, she has vomited twice, and now she looks weaker.
Suddenly, she has a forceful episode of vomiting, collapses, and becomes unresponsive.
An ABC assessment is performed. The airway is clear. Lexi is taking slow shallow breaths and has weak pulses at a rate of 20 bpm. She is taken immediately to the treatment table, where an ECG confirms a sinus bradycardia with a rate of 20 bpm. Shortly after, she stops breathing, the ECG shows asystole, and no pulse can be found.
What should you do first?
- give a bolus
-administer atropine
-start BLS
-defibrillate
-administer a vasopressin
BLS
. Although ALS interventions should be initiated as soon as possible, the first step for any patient in CPA is to start BLS.
Two staff members start BLS immediately on Lexi. During this first cycle of CPR, which of the following would be the most appropriate ALS intervention? - atropine and low dose epinephrine -atropine -low dose epinephrine -no ALS high dose epinephrine
Atropine and low dose epinephrine
. Lexi was documented to have sinus bradycardia just before she developed asystole, likely due to high vagal tone from her episode of vomiting. Vasopressor therapy is the highest ALS priority when treating patients with asystole. Because Lexi likely had a vagally mediated CPA, atropine should be administered at the same time as the epinephrine. Because Lexi had an ECG monitor in place at the time she developed CPA and the arrest rhythm (asystole) was diagnosed, you should not wait until the end of the next cycle to administer ALS therapies.
Borat: After 10 Minutes of CPR
Over the past two days, the owner has noted that Borat has been hiding and leaving piles of vomit around the house.
This morning the owner woke up and found Borat unresponsive, so she rushed him to the hospital. She reports that his appetite has decreased, but he was still drinking, urinating and defecating normally at home
She thinks Borat stopped breathing just a few minutes before arriving.
An ABC assessment was performed. Borat’s airway was clear. He was not breathing, and there was no apex beat. You initiated CPR. You were unsuccessful in placing an IV catheter, so an IO catheter was placed.
Throughout the first five cycles of CPR, Borat was in asystole. After 10 minutes of CPR, in addition to standard BLS and ALS therapy, what additional treatment would be most consistent with the RECOVER CPR guidelines?
-calcium gluconate
-atropine
-open chest CPR
-high dose epinephrine
-vasopressin
High dose epinephrine
. Vasopressors (epinephrine and vasopressin) are the mainstay of treatment for asystole and PEA, and anticholinergics, such as atropine, may also be helpful during CPR (in animals experiencing bradycardic arrest due to high vagal tone).
In cases of prolonged CPR, high-dose epinephrine may be administered. The use of sodium bicarbonate should be avoided unless there is a blood gas indicating severe acidosis, and routine use of calcium gluconate is not recommended unless you have documented low calcium.
After administering high-dose epinephrine, you obtain a venous blood gas. The results are shown here:
pH: 7.11 [7.35 - 7.45]
PvCO2: 48 mmHg [35 - 45]
BE: -10 mmol/L [0 - -4]
HCO3: 14 mmol/L [20 - 25]
Na: 151 mEq/L [149 – 156]
K: 9.7 mEq/L [3.8 – 5.1]
Cl: 112 mEq/L [110 – 119] In addition to standard BLS and ALS therapy and high-dose epinephrine, what additional treatment(s) for prolonged asystole would be most appropriate? -dexamethasone -sodium bicarbonate -low dose epinephrine and vasopressin -increase ventilation rate -calcium gluconate
calcium gluconate
If hyperkalemia is documented during CPR, treatment with 10% calcium gluconate IV (0.5 mL/kg) is recommended. This therapy normalizes the difference between resting membrane potential and threshold potential in cardiac cells. Sodium bicarbonate is only indicated in patients with severe acidemia (pH less than 7.0). Dexamethasone is only indicated in patients with documented adrenal insufficiency. Peripheral venous CO2 is a poor surrogate for arterial CO2 during CPR because poor peripheral blood flow reduces CO2 clearance. Ventilatory rate should be maintained at 10 breaths per minute regardless of the peripheral CO2 partial pressure. Finally, low-dose epinephrine and vasopressin are part of the standard ALS algorithm.
A patient in your hospital collapses suddenly and becomes apneic. You initiate BLS and attach an ECG monitor. At the end of the first cycle of BLS you pause chest compressions briefly and see a rhythm with repeated complexes at a rate of 126 per minute but do not feel a pulse or an apex beat. Your rhythm diagnosis is: VF Pulseless VT PEA Asystole Perfusing rhythm
Pulseless electrical activity
Asystole and pulseless electrical activity are non-shockable arrest rhythms and should not be treated with electrical defibrillation.
True or false
True
The goal of vasopressor therapy during CPR is to: Correct metabolic acidosis Achieve peripheral vasoconstriction Increase cardiac contractility Increase heart rate
Achieve peripheral vasoconstriction
In patients with bradyarrhythmias who suddenly develop cardiopulmonary arrest due to asystole, which of the following is true?
Defibrillation should be performed after one cycle of CPR
Atropine should be administered every cycle of CPR
Low dose epinephrine should be administered every cycle of CPR
High dose epinephrine should be administered during the first cycle of CPR
Atropine should be administered every other cycle of CPR
Atropine should be administered every other cycle of CPR
Which of the following may be the most beneficial during the first 10 minutes of CPR for patients with pulseless electrical activity that have severe academia? Vasopressin High-dose epinephrine Atropine Calcium gluconate
Vasopressin
After administering the first dose of a vasopressor during CPR in a dog with a non-shockable rhythm, if there is NO return of spontaneous circulation, how long should you wait before giving another dose of vasopressor? 2 minutes 4 minutes Vasopressors should not be repeated 6 minutes
4 minutes
Which if the following is a valid rationale for the use of sodium bicarbonate during CPR?
It improves the severe respiratory acidosis associated with CPA
It can be administered IT in patients without vascular access
It may improve the efficacy of vasopressin
It may improve the efficacy of epinephrine
start chest compressionsTrue
Which of the types of arrest rhythms is seen most commonly in dogs and cats?
Shockable
Non-shockable
non-shockable
A patient suddenly develops severe bradycardia during anesthesia for a distal limb mass removal. The ECG is attached and the animal rapidly progresses to asystole with no palpable pulses. According to the RECOVER CPR guidelines, what is the first treatment priority?
Start chest compressions
Administer low-dose epinephrine
Administer atropine
Connect the end tidal CO2 monitor
start chest compressions
High-dose epinephrine has been associated with an increased rate of ROSC during CPR, but has also been associated with a lower rate of survival to discharge. It is therefore recommended for use only in patients with prolonged CPA as a last ditch effort, and should only be administered with the understanding that it may decrease the likelihood of long-term survival.
False
True
True
What is the aim of defibrillation?
Because VF and VT are the result of abnormal pacing of groups of ventricular myocardial cells by the myocardial cells themselves rather than the natural pacemakers, the goal of electrical defibrillation is to depolarize as many of these cells as possible, driving them into their refractory period and stopping the ineffective activity. This means that the ultimate goal of electrical defibrillation is to stop all electrical and mechanical activity in the ventricles in order to permit the resynchronization of the electrical activity of the heart.
What does defibrillation do to the natural pacemakers?
If defibrillation is successful, the natural pacemakers (the SA node and/or the AV node) should then begin driving the myocardial cells, which may permit the return of a perfusing rhythm.
In other words, the goal of defibrillation is to stop the chaotic activity in order to permit synchronized contraction to occur, guided by either the sinus node or another of the natural cardiac pacemakers.
What are the three different types of defibrillation?
Three approaches to defibrillation have been described:
Electrical
Mechanical
Chemical
What is the best type of defibrillator?
There is extensive evidence showing that of the 3, electrical defibrillation is by far the most effective approach. Although we will discuss each of the options for defibrillation, if an electrical defibrillator is available, the other 2 types of defibrillation should never be used.
What is ventricular fibrillation?
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Recall that ventricular fibrillation is chaotic, uncoordinated electrical activity and contraction of ventricular myocardial cells, causing the heart to quiver. There is no cardiac output and no blood flow to the tissues.
What is electrical defibrillation?
Electrical Defibrillation
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Electrical defibrillation is accomplished by a device that delivers an electric shock to the heart via either chest paddles or adhesive patches for external defibrillation or internal paddles directly on the ventricles for internal defibrillation.
Wat is mechanical defibrillation
Mechanical Defibrillation
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Mechanical defibrillation may be attempted using a precordial thump. Unfortunately, recent studies have shown the precordial thump to have minimal effects on ventricular fibrillation, and this procedure is only recommended if an electrical defibrillator is not available. Do not thump if you have a defibrillator.
What is chemical defibrillation?
Chemical Defibrillation
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Chemical defibrillation using acetylcholine/potassium chloride, bretylium tosylate, lidocaine, and magnesium have been described in the experimental literature, but have not been shown to be useful in any clinical studies, and several have been shown to reduce the efficacy of electrical defibrillation. Therefore, chemical defibrillation is not recommended.
What is the most effective treatment for ventricular tachycardia and ventricular fibrillation.
Electrical defibrillation is the most effective treatment for VF and pulseless VT.
What are the two types of electrical defibrillators?
There are two types of electrical defibrillators:
Monophasic
Biphasic
Why is the applicability of automated electrical defibrillators unknown?
Automated electrical defibrillators (AED), which are widely available for use in sudden cardiac arrest in people, may potentially be useful in dogs, but because they deliver a standard adult human energy dose and were developed using ECGs collected from humans, their applicability in dogs and cats is unknown. In addition they use adhesive pads rather than paddles, requiring shaving before use. Therefore, the use of manual defibrillators with variable dosing is recommended for veterinary patients.
A large amount of energy is required to simultaneously depolarize the majority of ventricular myocardial cells with electrical current administered to the body surface. This large amount of energy can lead to myocardial injury. The lowest potentially effective defibrillator dose should always be used to minimize injury.
What type of defibrillator is preferred?
Biphasic defibrillators can successfully terminate VF at lower defibrillation energy than monophasic defibrillators, in turn leading to less myocardial injury. Therefore, biphasic defibrillators are preferred if they are available.
How can defibrillation lead to injury?
Although electrical defibrillation is the most effective treatment for VF and pulseless VT, it requires a large amount of electrical energy to be applied to the heart. This can lead to myocardial injury, the severity of which is proportional to the amount of energy applied.
What is included in the electrical defibrillation device?
Devices for delivering a shock to the patient include hand paddles, posterior paddle assemblies, pediatric hand paddle inserts, adhesive patches, and internal defibrillation paddles for use during open-chest CPR.
Where should hand paddles on an electrical defibrillator be placed on an animal receiving CPR?
When using hand paddles, they should be placed on opposite sides of the thorax approximately over the costochondral junction directly over the heart.
How should an animal be prepped for electrical defibrillation?
When using hand paddles, they should be placed on opposite sides of the thorax approximately over the costochondral junction directly over the heart. This allows the maximum amount of current to pass directly through the ventricles, increasing the likelihood of successful defibrillation. To accomplish this, the patient must be placed in dorsal recumbency. Sufficient electrode gel or paste must be applied to the paddles to ensure electrical contact with the skin, and animals with long hair may need to be shaved to achieve contact. The paddles must be pressed firmly against the chest wall to ensure contact. Alcohol, which is highly flammable, should never be used in place of electrode paste or gel
What is the benefit of a posterior paddle on an electrical defibrillator?
A posterior paddle assembly, which is a flat paddle replacement for one of the hand paddles, can improve the efficiency and safety of defibrillation, minimizing the interruption to compressions and eliminating the need to place the patient in dorsal recumbency.
The flat paddle is coated with gel or paste and placed under the patient’s thorax.
Defibrillation is then accomplished using a standard hand paddle on the upward facing chest wall.
Chest compressions can resume immediately while the posterior paddle is still in place.
What is the benefit of having paedatric hand paddles on an electrical defibrillator?
For cats and small dogs, pediatric hand paddle inserts are recommended if available, to direct more of the current through the heart. The large surface area of the adult paddles may lead to more current bypassing the heart through the skin and subcutaneous and muscle tissues, decreasing effective dose delivery. If pediatric paddles are not available, use of the adult paddles is acceptable.
What are the downfalls of using adhesive defibrillation patches?
Adhesive defibrillation patches can be used in dogs and cats but they require the chest to be shaved in order for contact to be achieved. This may result in prolonged delays in chest compressions, and should only be used if hand paddles or a posterior paddle assembly are not available.
How do you use internal dWhat is the elecefibrillation paddles?
During open-chest CPR, defibrillation is accomplished using internal defibrillation paddles. These paddles are much smaller than devices used for external defibrillation. It is also important to use a lower dosing scheme for internal defibrillation to avoid serious myocardial injury. If you have internal paddles, be sure that your chart includes a separate dosing scheme for internal defibrillation.
Before use, internal defibrillation paddles may be wrapped in 0.9% saline-soaked gauze to facilitate contact with the ventricles, if desired. The paddles should be placed on either side of the ventricles and firmly pressed against the heart to facilitate contact. Between uses, the paddles should be sterilized according to manufacturer recommendations and kept in sterile packaging in the crash cart.
What is the electrical phase?
Electrical Phase
During the first four minutes after the onset of CPA, known as the electrical phase, ATP stores in the heart are usually sufficient to sustain cell membrane potentials and metabolic demands, which minimizes ischemic damage.
What is the circulatory phase?
Circulatory Phase
The next six minutes are called the circulatory phase, during which reversible ischemic injury due to ATP depletion occurs
What is the metabolic phase?
Metabolic Phase
After 10 minutes without perfusion, the metabolic phase begins, which is characterized by potentially irreversible ischemic injury.
Is early electrical defibrillation advised?
Early electrical defibrillation is associated with better outcomes, but in some cases, one full cycle of BLS should be administered before defibrillating.
Once circulation to the tissues ceases in a patient in CPA, ischemic injury to the tissues begins.
If a patient has a witnessed monitored arrest and has ventricular fibrillation or pulseless ventricular tachycardia should electrical defibrillation start?
Witnessed, Monitored Arrests
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Patients experiencing sudden CPA while being monitored with an ECG and noted to convert from a perfusing rhythm into VF or pulseless VT are in the initial electrical phase and have experienced minimal ischemic injury. The heart is capable of re-establishing a perfusing rhythm quickly if the VF or pulseless VT can be terminated immediately. Therefore, BLS should be initiated and continued only long enough to charge the defibrillator. Once the defibrillator is charged, the patient should be defibrillated immediately. After the defibrillation, BLS should be restarted and continued for a full cycle before rechecking the ECG, unless other signs of ROSC develop, such as a sudden increase in EtCO2 or development of palpable pulses.
If a patient has an unwitnessed monitored arrest and has ventricular fibrillation or pulseless ventricular tachycardia should electrical defibrillation start straight away?
Unwitnessed Arrests
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Patients discovered in CPA with an initial arrest rhythm of VF or pulseless VT diagnosed before initiation of BLS should receive a full two-minute cycle of BLS before defibrillation. Because of the likelihood that the patient with an unwitnessed arrest has entered the circulatory or metabolic phase, a full cycle of BLS will provide perfusion to the heart and restoration of ATP stores, increasing the likelihood of a successful defibrillation. Shocking an ischemic heart depleted of ATP is unlikely to restore a perfusing rhythm and will result in additional myocardial injury.
Note that if the RECOVER algorithm is being followed, this circumstance should not occur, as BLS should be started before an ECG monitor is attached.
If a patient has a Shockable Rhythm Diagnosed during an Inter-cycle Pause in BLS should electrical defibrillation start straight away?
Shockable Rhythm Diagnosed during an Inter-cycle Pause in BLS
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If a shockable rhythm is diagnosed after a full two-minute cycle of BLS, during the brief inter-cycle pause in chest compressions, BLS should be resumed immediately and continued only as long as it takes to charge the defibrillator, at which time BLS should be paused and the patient defibrillated. Because perfusion of the heart has been provided by the BLS delivered during the previous cycle, the patient is in the electrical phase and immediate defibrillation is warranted.
The goal of electrical defibrillation is to stop chaotic ventricular activity in the heart by pushing as many of the ventricular myocardial cells into their refractory period as possible. Given that the goal is to stop the heart, what do you think you should do after every electrical defibrillation?
If electrical defibrillation is successful, there will be no blood flow out of the heart, so it’s very important to restart BLS immediately after the electrical defibrillation attempt.
Why is it important to start BLS after electrical defibrillation?
After each defibrillation attempt, BLS should be resumed immediately and continued for another two-minute cycle. The patient can be assessed for evidence of ROSC during this cycle by pulse palpation and EtCO2 monitoring, but resumption of BLS should not be delayed to interpret the ECG, as direct conversion to a perfusing rhythm may not have occurred and longer pauses in chest compressions are associated with worse outcomes. Note that this is in contrast to older CPR guidelines, which recommended three stacked shocks in patients with VF that did not respond to an initial defibrillation attempt. More recent studies have shown poorer outcomes with a stacked shock approach, likely due to the lack of perfusion during the repeated defibrillation attempts in the absence of continued BLS.
How often should defibrillation be repeated if a shockable rhythm remains?
Note that, in contrast to drug administration for the non-shockable rhythms, which is repeated every other cycle of BLS (every 3-5 minutes), defibrillation for the shockable rhythms should be repeated every cycle of BLS (every 2 minutes).
If a patient is still in VT or pulseless VT at the end of a 2 minute cycle what should be done?
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If the patient is still in VF or pulseless VT at the end of the two-minute cycle of BLS, the defibrillator dose may be increased by 50% and the patient defibrillated again, followed immediately by another two-minute cycle of BLS. The dose may be increased each time defibrillation is attempted at the end of each two-minute cycle of BLS, to a maximum dose of 10 J/kg. The evidence for dose escalation is stronger for monophasic defibrillators than for biphasic defibrillators. Two-minute cycles of BLS followed by electrical defibrillation should be repeated until ROSC is achieved, conversion to a non-shockable rhythm (asystole or PEA) occurs, or the CPR attempt is abandoned.
Should alcohol be used with an electrical defibrillator, why?
Avoid Alcohol
Alcohol, which is occasionally used to facilitate ECG recording, should be avoided during CPR, as it is highly flammable and could cause a skin burn or the fur to catch fire if VF or pulseless VT develops and electrical defibrillation is indicated. Electrode gels and pastes are non-flammable and should be used during CPR to improve ECG electrode contact.
What does the call out clear mean when using the electrical defibrillator?
Call Out “CLEAR”
The individual operating the defibrillator should be careful to call out “CLEAR” prior to delivering the charge, and should ensure that all personnel are away from the patient and treatment table before delivering the shock. “CLEAR” is the signal to stop touching the patient OR any object that might conduct electricity, such as metal treatment tables or pools of fluid making contact with the patient. When the person operating the defibrillator calls out “CLEAR”, it means that they are confident that they can maintain the animal in the same position (i.e., dorsal recumbency) when everyone else lets go of the animal.
Why should you avoid contact with an animal receiving electrical defibrillation?
Avoid Contact
The person administering the shock is at the highest risk from the procedure. When two hand paddles are used, care should be taken to avoid contact with the patient’s limbs, as they have a tendency to rest on the rescuer when the patient is held in dorsal recumbency. The use of exam gloves may reduce the risk of shock, but care must be taken to prevent electrode gel or fluid from forming a bridge over the glove to the rescuer’s forearm. In addition, the rescuer should avoid leaning on the treatment table, which could also form a conductive path between the patient and the rescuer.
How much energy does a precordial thump provide as mechanical defibrillation?
The precordial thump delivers 5–10 joules of energy to the heart.
Where do you apply mechanical defibrillation and how much force needs to be used?
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A precordial thump is performed by striking the chest directly over the heart. The location of the heart can be estimated by pulling the elbow caudodorsally over the chest until it is roughly at the level of the costochondral junction. This will be over the third to fifth intercostal space.
In medium to large breed dogs, the rescuer should strike the chest with as much force as possible. In small dogs and cats, care should be taken to not overly traumatize the heart.
What is the goal of anti-arrhythmic therapy?
The goal of anti-arrhythmic therapy is to terminate the pathological rhythm by acting on specific parts of the cardiac cycle. While anti-arrhythmic therapies are commonly used in patients with ectopy, their role in CPR is less well established.
What are the two most commonly used anti-arrhythmia drugs used for pulseless VT and VF?
The two most extensively studied anti-arrhythmic drugs for prolonged pulseless VT and VF are Amiodarone and Lidocaine.
What is the superior anti-arrhythmic drugs to use with prolonged pulseless VT and VF?
The two most extensively studied anti-arrhythmic drugs for prolonged pulseless VT and VF are Amiodarone and Lidocaine. Amiodarone is believed to be the most effective for increasing the rate of ROSC with electrical defibrillation in patients with pulseless VT or VF. However, lidocaine may be considered as an alternative if amiodarone is not available, as it is much more widely available in veterinary practices, and specific veterinary benefits of amiodarone over lidocaine have not been established.
Why should anti-arrhythmic drugs only be used after 10 minutes of refractory VF or pulseless VT?
Remember that all anti-arrythmic drugs have the potential to be arrhythmogenic, so administration of anti-arrhythmic therapy in conjunction with electrical defibrillation should only be considered in patients with refractory VF or pulseless VT lasting at least 10 minutes (5 cycles of BLS).
What is the indication to use amiodorone?
It is useful for treatment of stable ventricular tachycardias as well as during CPR in conjunction with electrical defibrillation for prolonged VF/pulseless VT
What drug class is Amiodorone in and what does it do?
Amiodarone is a class III anti-arrhythmic agent and prolongs phase 3 (the repolarization phase) of the action potential in cardiac cells. However, it has other anti-arrhythmic properties as well, such as beta blocking and potassium-channel blocking in the SA and AV nodes, slowing the pacemakers and atrial-ventricular conduction.
What is the dose of Amiodorone?
Dosing
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During CPR, amiodarone may be given slowly IV/IO over 1–2 minutes at a dose of 5 mg/kg. If possible, it should be diluted to 0.5 mg/ml with D5W prior to administration. It should not be given IT.
What are the side effects of Amiodorone?
Side Effects
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The major potential side effect is anaphylaxis, leading to hypotension and severe hives (urticaria) due to the vehicle in some formulations of the drug. This is less likely with the aqueous amiodarone solution, which is the preferred formulation for use in dogs. Patients demonstrating these signs upon ROSC should be given diphenhydramine (2 mg/kg IM) and dexamethasone SP (0.1 mg/kg IV). Vasopressors may be considered if hypotension develops. Newer preparations are less likely to cause anaphylaxis.
What should be used as an antiarrhythmic if Amiodorone is not available?
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In people, prolonged VF and pulseless VT respond better to amiodarone than to any other drug, or to repeated attempts at electrical defibrillation without additional antiarrhythmic therapy. The clinical utility of amiodarone in veterinary patients is unknown, but there is some experimental evidence that it is beneficial in dogs with prolonged VF/pulseless VT.
If available, in prolonged VF/pulseless VT, amiodarone should be administered. If amiodarone is not available, lidocaine may be considered in these patients.
What drug class is lidocaine in and how does it work as an anti-arrhythmic drug?
Lidocaine is a class 1B antiarrhythmic that blocks fast sodium channels in the ventricular myocardium, shortening the action potential and slowing the ventricular rate.
What are the indications to use lidocaine as an antiarrhythmic drug?H
Like amiodarone, lidocaine is useful for treatment of stable ventricular tachycardias as well as during CPR in conjunction with electrical defibrillation for prolonged VF/pulseless VT. In unstable VT, lidocaine administration may increase the fibrillation threshold, preventing deterioration of VT into VF.
How can lidocaine affect defibrillation?
One study using monophasic defibrillation showed that after VF developed, treatment with lidocaine increased the energy required to successfully electrically defibrillate the dogs. More recent data in humans and pigs showed that lidocaine actually decreased the defibrillation threshold with biphasic defibrillation, resulting in successful defibrillation with lower energy in patients with prolonged VF.
Due to lidocaine’s widespread availability, it is a reasonable drug to consider for adjunctive therapy for prolonged VF/pulseless VT (longer than 10 minutes, or 5 cycles of BLS) if biphasic defibrillation alone is not successful despite high-quality BLS and ALS interventions. If a monophasic defibrillator is being used, lidocaine may be given, but it may require higher defibrillation energies to be effective
What do vasopressors do during CPR?
During CPR, vasopressors provide peripheral vasoconstriction, which diverts blood from the periphery to the core, improving myocardial perfusion
Why are catecholamines contraindicated in VT and VF?
During CPR, vasopressors provide peripheral vasoconstriction, which diverts blood from the periphery to the core, improving myocardial perfusion. However, peripheral vasoconstriction increases afterload, potentially decreasing cardiac output. Catecholamines like epinephrine can potentially worsen arrhythmias like VT and VF. For this reason, vasopressors are only recommended in patients with prolonged VF and pulseless VT (greater than 10 minutes, or 5 cycles of BLS).
Why do you start off giving lose doses of epinephrine?
Epinephrine is the most commonly used vasopressor during CPR, but as described in Module 2 (Treating the Patient: Asystole and PEA), ephinephrine is an agonist at all adrenergic receptors. Therefore, in addition to peripheral vasoconstriction, substantial β-1 agonism occurs, which has the potential to worsen ventricular arrhythmias in patients with VF/pulseless VT. Therefore, low-dose epinephrine (0.01 mg/kg IV/IO/IT every 3–5 minutes) is reserved for patients with VF/pulseless VT that has been refractory for at least five cycles of BLS and electrical defibrillation (longer than 10 minutes). High dose epinephrine (0.1 mg/kg) is not recommended for treating shockable arrest rhythms because of the potential to worsen the arrhythmia due to the β-1 effects
Why is vasopressin the preferred drug for use in CPR?
Vasopressin (0.8 IU/kg IV/IO/IT every 3–5 minutes) may be preferable to epinephrine in patients with prolonged VF/pulseless VT, as it does not require a normal pH for efficacy, and it acts only as a vasopressor, without the β-1 effects that may worsen ventricular arrhythmias in these patients. However, studies comparing epinephrine to vasopressin for patients with prolonged VF/pulseless VT are lacking.
Because the best ALS therapies for the shockable and non-shockable rhythms differ and the ECG is highly susceptible to motion artifact, if the team does not agree on the rhythm diagnosis during the pause in chest compressions at the end of a BLS cycle, resumption of chest compressions should be delayed until all members of the team examine the ECG and agree upon a rhythm diagnosis.
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False
A 9 year old Doberman Pinscher presents to your clinic for weakness, cough and lethargy. He is non-ambulatory, and was carried into the treatment area. You connect an ECG and see wide complexes at a rate of 242 per minute although his pulse rate is only 96 per minute. How would you treat this dog?
Perform a full 2 minute cycle of chest compressions
Because there are pulses, no treatment is necessary
Administer a slow IV bolus of lidocaine
Start chest compressions while charging the defibrillator, then defibrillate
Bolus 30 ml/kg IV of 0.9% saline for hypotension.
Administer a slow IV bolus of lidocaine
At the end of a cycle of BLS, you evaluate the ECG and diagnose ventricular fibrillation. You continue chest compressions while charging the defibrillator and then pause compressions to administer the shock. What is the correct next step?
Immediately resume chest compressions and defibrillate again if the patient is still in VF at the end of the next BLS cycle.
Immediately start the next cycle of BLS and defibrillate every other cycle as long as a shockable rhythm is still present.
Evaluate the ECG and shock 2 more times (“stacked shocks”) if the patient is still in VF, then restart BLS after the third shock.
Evaluate the ECG and administer amiodarone if the patient is still in VF.
Immediately resume chest compressions and defibrillate again if the patient is still in VF at the end of the next BLS cycle.
Although biphasic electrical defibrillators are more efficacious for treating VF and pulseless VT than monophasic defibrillators, the same dosing chart may be used for both types.
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A patient has been in pulseless VT for 5 cycles of CPR, meeting the criteria for prolonged pulseless VT. You have been treating with good quality BLS and electrical defibrillation per the RECOVER guidelines. Which of the following would be a useful additional therapy in this patient?
Amiodarone IV
Dexamethasone SP IV
Atropine IV
A precordial thump
Amiodarone IV
The goal of defibrillation is to reset the pacemakers in the SA node and establish a perfusing rhythm, so it may be useful in patients with prolonged asystole.
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True
False
All of the following are important aspects of electrical defibrillator safety EXCEPT:
Calling out “Clear” and verifying that all personnel are away from the patient
Standing away from the treatment table, especially if it is metal
Being sure not to touch the patient during defibrillation
Using alcohol on ECG clips
Using alcohol on ECG clips
When performing a precordial thump on a cat, it is important to strike the chest directly over the heart with as much force as possible to stun as many ventricular myocardial cells as possible.
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False
False
Low-dose epinephrine should be administered every other cycle of CPR in all patients with shockable arrest rhythms.
True
False
False
