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Managing Cardiopulmonary Arrest
Christopher Norkus, BS, CVT, VTS (ECC), VTS (Anesthesia)
C
ardiopulmonary arrest (CPA) is characterized by abrupt,
complete failure of the respiratory and circulatory systems.
The lack of cardiac output and oxygen delivery to tissues
(DO2) can quickly cause unconsciousness and systemic cellular
death from oxygen starvation. If left untreated, cerebral hypoxia
results in complete biologic brain death within 4 to 6 minutes of
CPA.1,2 Therefore, prompt cardiopulmonary cerebral resuscitation
(CPCR) is imperative. Veterinary technicians can play a key role
in ensuring that patients receive this treatment.
Causes and Clinical Signs
In dogs and cats, common causes of CPA include anesthetic
complications; vagal stimulation; hypovolemia; severe trauma,
such as pneumothorax; unstable cardiac arrhythmias, such as
unstable ventricular tachycardia; severe electrolyte disturbances,
such as hyperkalemia; cardiorespiratory disorders, such as congestive
heart failure, hypoxia, or pericardial tamponade; and debilitating
or end-stage diseases, such as sepsis or cancer.
Potential signs of impending CPA include dramatic changes in
breathing effort, rate, or rhythm (e.g., agonal breathing, decreased
rate, sudden increased rate); the absence of a pulse; significant
hypotension (i.e., systolic blood pressure <50 mm Hg [normal:
>90 to 100 mm Hg]); irregular or inaudible heart sounds; changes
in the heart rate or rhythm; change in mucous membrane color
(e.g., white or cyanotic); fixed, dilated pupils; distressed vocalizations;
and collapse.
Assessment of the patient is crucial if CPA is suspected. Before
CPCR is initiated, it is essential to evaluate the patient’s responsiveness, breathing pattern, and pulse because patients in arrest
are nonresponsive and apneic, with no detectable pulse.
Cardiopulmonary Cerebral Resuscitation
CPCR is initiated in three stages: basic life support (BLS), advanced
life support (ALS), and postresuscitative care.3 Adopted from
human emergency medicine, BLS involves establishing an open
and clear airway, providing assisted ventilation, and performing chest
compressions. These steps are often called the ABCs—airway,
breathing, and circulation. ALS includes advanced care such as
establishing venous access, interpretation of an electrocardiogram
(ECG), drug administration, and defibrillation and is typically
performed by credentialed veterinary technicians, veterinarians,
or both. Postresuscitative care includes intensive monitoring as
well as cardiovascular and ventilatory support.
Vetlearn.com | April 2011 | Veterinary Technician
CPCR Stage 1: Basic Life Support
Airway management involves extending the patient’s neck to
straighten the airway and pulling the patient’s tongue forward.
The veterinary staff should quickly examine the upper airway
and initiate suctioning, if necessary. All foreign material or vomit
observed in the patient’s mouth should be cleared immediately.
If the patient’s airway is fully obstructed, abdominal thrusts
and finger sweeps of the pharynx can help dislodge the obstruction.
An emergency tracheotomy, which is performed by a veterinarian,
may be necessary if the airway obstruction is not immediately
resolved. Insertion of a large-gauge needle or intravenous (IV)
catheter directly into the trachea below the obstruction, along
with oxygen administration, can be useful while the tracheotomy
is being performed. In some cases, material fully obstructing the
airway (e.g., a ball) can be manually removed with long hemostats
or Doyen intestinal clamps.
After the patient’s airGlossary
way has been cleared, an
endotracheal tube should
Hemothorax—accumulation of blood
be placed. Tube placement
in the pleural cavity
should be confirmed and the
tube secured and cuffed. The
Hyperkalemia—an abnormally high
patient should then be venconcentration of potassium ions in
tilated with 100% oxygen.
the blood
Proper ventilation is a
critical component of BLS.
Hypovolemia—a decreased blood
Based on the most recent
volume
published recommendations,
Hypoxia—deficiency in the amount of
veterinary patients should
oxygen reaching the body tissues
receive 100% oxygen at a rate
of 10 to 24 breaths/min.4,5
Pneumothorax—accumulation of air
In humans, more frequent
or gas in the pleural cavity
ventilation has been shown
to be significantly detriThoracentesis—removal of fluid or air
mental because it can result
from the chest through a needle or tube
in decreased myocardial
and cerebral perfusion.6
Transcutaneous pacing (also called
Therefore, choosing a lower
external pacing)—a temporary means
rate from the range of 10
of pacing a patient’s heart by delivering
to 24 breaths/min may be
pulses of electric current through the
advised; these rates may
patient’s chest, which stimulates
be reexamined in future
contraction of the heart
literature.
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Managing Cardiopulmonary Arrest
BOX 1. Impedance Threshold Devices
The development of impedance threshold devices (ITDs) has shown promise
in both human and animal models.19 The ITD is a small, inexpensive device
that is placed on the proximal end of an endotracheal tube during resuscitation
to create an increase in negative pressure during the chest-recoil phase of
chest compression. An increase in negative pressure creates a vacuum that
results in more blood being pulled into the heart and, therefore, more blood
output during the next compression. ITDs include a timing light that helps the
rescuer ventilate the patient at the proper rate to avoid hyperventilation.
Figure 1. An Ambu bag. Courtesy of David Liss, RVT, VTS (ECC).
Veterinary patients can be easily and safely ventilated with an
Ambu bag (FIGURE 1) or bag-valve mask. Using an anesthesia unit
can be slow and ineffective because the pop-off valve must be
opened and closed repeatedly. Peak airway pressure should be
<20 cm H2O.4 Lack of chest wall motion, poor ventilation, or absence
of lung sounds should prompt an immediate search for a poorly
positioned tube or a severe pleural space disorder, such as pneumothorax. In these cases, thoracentesis or thoracotomy performed by a veterinarian may be necessary.
Acupuncture has also been used to help treat CPA and respiratory
depression.7 Needling the acupuncture point GV26 can help
stimulate respiration and increase cerebral oxygen.8–10 This acupoint
can be stimulated by inserting a regular 25-gauge needle or acupuncture needle into the nasal philtrum to a depth of approximately
10 to 20 mm and performing jabs in a hen-pecking motion while
monitoring for improvement in respiration.8
The goal of circulatory support during CPCR is to maximize
myocardial and cerebral perfusion. Chest compressions should be
performed immediately in patients without a detectable heartbeat.
External cardiac massage at a rate of 80 to 120 compressions/min
is recommended,6 but higher rates within that range seem to
work better.11 Small patients (<15 lb [7 kg]) should receive compressions directly over the heart (cardiac pump theory), whereas
larger patients should receive more caudal compressions that are
directed over the widest part of the chest (thoracic pump theory).
The cardiac pump theory asserts that arterial blood flow is a
result of direct compression of the ventricles and, therefore,
makes sense in small patients with pliable chest walls. Closed-chest
compressions in large patients, however, generally are inadequate
in compressing the ventricles. Therefore, the thoracic pump theory,
which suggests that forward blood flow in larger patients is the
result of a generalized increase in intrathoracic pressure, is used
in these patients. Ideally, two technicians should perform interposed abdominal compressions, in which alternate compressions
of the cranial abdomen and the chest are completed at a rate of 70
Vetlearn.com | April 2011 | Veterinary Technician
to 90 compressions/min. This has been shown to increase cardiac
output.12–14
Based on the “2010 American Heart Association (AHA)
Guidelines for Cardiopulmonary Resuscitation and Emergency
Cardiovascular Care”15 and the “2010 International Consensus
on Cardiopulmonary Resuscitation and Emergency Care Science
With Treatment Recommendations,”16 rescuers performing chest
compressions should push hard and fast, allow full chest recoil
after each compression, and minimize interruptions in compressions.
It is critical for chest compressions to be continuous after they
have begun.
Guidelines for open-chest internal cardiac massage (ICM),
which is performed by a veterinarian, typically recommend its
immediate use in all patients >40 lb (18 kg); in patients after 10
minutes of unsuccessful CPCR, regardless of their size; and in all
cases of trauma and/or hemorrhage, such as patients with pneumothorax, hemothorax, or cardiac tamponade.5,17 ICM allows
direct visualization of the heart, aortic compression or temporary
ligation, and internal defibrillation. In addition, ICM can increase
cardiac output, blood pressure, coronary perfusion pressure, and
cerebral perfusion pressure compared with closed-chest CPCR and
has been associated with increased return of spontaneous circulation and improved neurologic outcomes in animal models.11,18
The veterinary staff should regularly assess the effectiveness of
CPCR by palpating for the presence of pulses during compressions
and by using a Doppler ultrasound transducer; however, compressions should never be stopped for an assessment. With sufficient water-based lubricant, a Doppler transducer can be placed
directly over one of the patient’s open eyes. The presence of a
“swooshing” wave sound from the Doppler unit during concurrent
chest compressions can provide a crude estimate of whether forward blood flow is reaching the brain. If chest compressions are
not generating adequate forward blood flow, either the patient
should be repositioned and the resuscitation technique changed
to increase intrathoracic pressure (BOX 119) or ICM should be
considered.
CPCR Stage 2: Advanced Life Support
Establishing venous access is important but should never interfere
with chest compressions or defibrillation. Venous access can be
established by using methods such as intraosseous catheter placement and venous cutdown, in which a small opening is created in
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Managing Cardiopulmonary Arrest
BOX 2. Treating Arrhythmias
Treatment of cardiopulmonary arrest depends on the type of arrhythmia, which
can be effectively differentiated on an electrocardiogram (ECG) only. The two most
common arrhythmias in veterinary patients are ventricular asystole and pulseless
electrical activity (PEA), also known as electromechanical dissociation. Ventricular
fibrillation (VF), the most common arrhythmia in humans, is not as common in cats
and dogs.24 This may be partly due to the fact that humans commonly experience
cardiac arrest for different reasons (i.e., myocardial infarction) than veterinary patients.
Ventricular Asystole
Asystole, also known as flatline, is the absence of electrical or mechanical activity from
the heart. A rare P wave may be observed, but no QRS complexes are seen (FIGURE A).
Transcutaneous electrical pacing (Glossary) is immediately initiated in human
patients with asystole, but it has not gained widespread use in veterinary patients.
Routine veterinary treatment includes IV epinephrine administered at 0.01 to 0.02
mg/kg q3–5min and IV atropine administered at 0.02 to 0.05 mg/kg q3–5min.21
Routine veterinary treatment includes administration of IV epinephrine at 0.01 to
0.02 mg/kg q3–5min and IV atropine at 0.04 to 0.05 mg/kg q3–5min.21 The “2010 AHA
Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care” do
not advocate the routine use of atropine to manage human PEA because the drug has
not proved to be of significant benefit for this purpose.15 One dose of IV vasopressin
administered at 0.8 mg/kg is also likely to be beneficial in treating PEA.25 The use of
different therapies, such as naloxone, dexamethasone, and calcium, to help treat PEA has
been advocated. However, little published information supports regular use of these agents.
Ventricular Fibrillation
In patients with VF, the ECG wave form is erratic and chaotic. No clear P waves,
QRS complexes, or T waves are observed (FIGURE C).
Treating VF involves immediate electrical defibrillation. An initial shock of 3 to
5 J/kg is recommended; if the heart rhythm does not respond, two additional shocks,
each at a 50% higher setting than the previous one, should be given in immediate
succession. If, after the three progressively higher-voltage shocks,
conversion to a stable rhythm is not successful, chest compressions
and ventilation are continued for 2 minutes.21 Low-dose epinephrine
at 0.01 mg/kg and vasopressin at 0.8 U/kg are then administered.
These drugs can improve the likelihood of successful defibrillation.
Defibrillation is then resumed at 5 to 10 J/kg, followed by
administration of an additional drug, such as amiodarone,
Figure A. This ECG of a patient with ventricular asystole is a flatline showing no QRS complexes
lidocaine, magnesium chloride, or procainamide. After each new
and a rare P wave.
drug has been administered, defibrillation is again attempted at
the 5- to 10-J/kg setting to restore a normal perfusing rhythm.21
The “2010 AHA Guidelines for Cardiopulmonary Resuscitation
and Emergency Cardiovascular Care” recommend that health
care providers continue cardiopulmonary cerebral resuscitation
(CPCR) for 2 minutes after initial defibrillation before attempting
defibrillation a second time or administering drug therapy in
Figure B. This ECG of a patient with PEA looks relatively normal, reflecting the presence of
human patients.15 These recommendations are based on the
electrical activity. P waves, QRS complexes, and T waves are present.
understanding that biphasic defibrillators are readily used in
human medicine and have a high initial defibrillation rate.
Because biphasic defibrillators are not yet frequently used in
veterinary medicine, human literature based on older AHA
guidelines may be more applicable to treating dogs and cats.
Biphasic defibrillation has been documented in small animal
patients and will likely become the preferred method of small
Figure C. This ECG of a patient with VF shows the typical erratic pattern with no distinct P waves,
animal defibrillation in the future.26 When this more effective
T waves, or QRS complexes. Courtesy of Dianne Hudson, RVT, VTS (Anesthesia), Oklahoma State
method of defibrillation becomes commonplace, it may make
University College of Veterinary Medicine.
sense to continue chest compressions for a longer period.
It is difficult to successfully treat VF without a defibrillator.
A sharp precordial thump administered to the chest wall may convert VF to a sinus
The “2010 AHA Guidelines for Cardiopulmonary Resuscitation and Emergency
rhythm in small patients but is unlikely to be effective in larger patients. Although
Cardiovascular Care” do not advocate routine use of atropine to manage human
pharmacologic defibrillation using agents such as potassium chloride, insulin–
asystole because the drug has not proved to be of significant benefit for this
dextrose, and acetylcholine has been suggested, their use is almost never effective.
purpose.15 One dose of IV vasopressin administered at 0.8 U/kg should also be
Currently, the use of doxapram for respiratory arrest is not recommended. In
administered early into the arrest.25
human preterm infants, the drug has been shown to increase cerebral oxygen
demand and, therefore, potentially worsen outcomes.27
Pulseless Electrical Activity
The ECG of patients with PEA is relatively normal, reflecting the presence of
Sodium bicarbonate should only be administered during CPCR to manage
electrical activity in the heart. Consequently, P waves, QRS complexes, and T
severe metabolic acidosis diagnosed before the arrest, preexisting hyperkalemia,
waves may be observed (FIGURE B). However, in patients with PEA, lack of
or metabolic acidosis generated by prolonged CPCR efforts (>10 minutes) and
anaerobic metabolism in hypoxic tissues. The routine use of calcium during
mechanical activity in the heart prevents effective forward perfusion to the body,
CPCR is no longer advised. Its use may be justified in patients with hyperkalemia
resulting in the absence of palpable pulses. (It is important to remember that a
or hypocalcemia or affected by a calcium channel blocker overdose. Routine use
normal ECG does not mean that a patient is alive; veterinary students are often
may potentiate cellular damage secondary to ischemia.28
reminded of this to ensure that they look at their patients.)
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Managing Cardiopulmonary Arrest
the skin to allow passage of a needle or cannula into a vein. The
jugular vein typically yields well to catheterization during CPA
and provides the shortest transit time for drugs to reach the heart.20
After venous access has been established, aggressive fluid administration should be considered if hypovolemia existed before the
CPA or if the patient is experiencing blood loss. However, overzealous fluid administration in patients with normal body fluid
volume may be detrimental. Fluid resuscitation can include
administration of hypertonic saline, crystalloids, colloids, blood
products, and hemoglobin-based oxygen-carrying solutions.20
If an IV catheter cannot be placed initially, emergency drugs
(e.g., lidocaine, epinephrine, atropine, vasopressin, naloxone)
can be administered through an endotracheal tube.20 Typically, a
long red rubber catheter is inserted down the tube, and drugs are
administered through the catheter. Drug doses administered this
way are normally increased two- to threefold and are followed by
a small saline “chaser” to ensure successful drug passage into the
lungs. For example, the dose for IV atropine is 0.02 mg/kg, but if
it is administered through the endotracheal tube, the dose would
be 0.04 to 0.06 mg/kg.21
Intracardiac injection of medication is contraindicated, especially
during closed-chest CPCR. Inaccurate injection and complications,
such as vessel laceration and hemorrhage, are common.22,23
Accurate ECG interpretation, which determines the specific
arrhythmia the patient is experiencing (BOX 220–28), is necessary
before CPA can be treated. After the type of arrhythmia has been
established, drug administration and defibrillation can be initiated.
If CPA occurs as a result of anesthesia, all anesthetic agents must
be immediately discontinued and their effects reversed, if possible.
Unfortunately, most patients in CPA cannot be resuscitated
even if CPCR is performed perfectly. End-tidal carbon dioxide
measurements >15 mm Hg are reportedly associated with higher
survival rates.29 Other types of arrhythmia can usually be treated
until they progress to asystole, unless the patient’s owner declines
further resuscitation efforts.
CPCR Stage 3: Postresuscitative Care
Patients that are restored to a perfusing cardiac rhythm commonly
experience rearrest—often within minutes to several hours—
especially if the original cause of the CPA has not been identified.
Therefore, resuscitated patients usually require substantial cardiovascular and ventilatory support during the period following
CPA. Mild hypothermia after resuscitation from CPA decreases
cerebral oxygen demand and has been shown to improve outcomes in dogs.30 Inducing mild hypothermia in patients could be
considered a therapeutic option. In human patients, hyperglycemia
has been shown to be associated with worse neurologic outcomes
and should, therefore, be avoided after CPA.31
Poor perfusion during CPA may also precipitate brain injury,
disseminated intravascular coagulation, gut reperfusion syndrome,
and renal failure. Therefore, intensive monitoring and aggressive
supportive care are required to optimize management of blood
pressure, cardiac output, oxygenation, ventilation, and vital organ
perfusion.30,31
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Conclusion
After CPA, the success rate for recovery of veterinary patients is
generally poor.32–34 A 1-week survival rate of <4% has been
reported for cats and dogs that received CPCR following full a
rrest.31 However, functional recovery has been reported in most
animals that survive CPA.35
Based on current research, resuscitation appears to be successful
in patients that are treated quickly; have a reversible underlying
disease process, such as anesthetic overdose, upper airway obstruction, hemorrhage, or electrolyte abnormalities; and, ideally,
are not in full CPA.24,27,28
References
1. Safar P. Cerebral resuscitation after cardiac arrest: a review. Circulation 1986;74
(6 pt 2):IV138-153.
2. Safar P. Resuscitation from clinical death: pathophysiologic limits and therapeutic
potentials. Crit Care Med 1988;16(10):923-941.
3. Pablo LS. Current concepts in cardiopulmonary resuscitation. World Small Anim Vet
Assoc World Congr Proc 2003.
4. Kruse-Elliott KT. Cardiopulmonary resuscitation: strategies for maximizing success.
Vet Med 2001;16(1):51-58.
5. Henik RA. Basic life support and external cardiac compressions in dogs and cats.
JAVMA 1992;200(12):1925-1931.
6. Plunkett SJ, McMichael M. Cardiopulmonary resuscitation in small animal medicine:
an update. J Vet Intern Med 2008;22(1):9-25.
7. Schoen AM. Veterinary medical acupuncture in critical care medicine. World Small
Anim Vet Assoc World Congr Proc 2003.
8. Looney AL. Current thoughts on cardiopulmonary arrest and resuscitation. Atlantic
Coast Vet Conf Proc 2001.
9. Janssens L, Altman S, Rogers PA. Respiratory and cardiac arrest under general anaesthesia: treatment by acupuncture of the nasal philtrum. Vet Rec 1979;105(12):273-276.
10. Davies A, Janse J, Reynolds GW. Acupuncture in the relief of respiratory arrest. N Z
Vet J 1984;32:109-110.
11. Kern KB, Sanders AB, Badylak SF, et al. Long-term survival with open-chest cardiac
massage after ineffective closed-chest compression in a canine preparation. Circulation
1987;75(2):498-503.
12. Voorhees WD 3rd, Ralston SH, Babbs CF. Regional blood flow during cardiopulmonary resuscitation with abdominal counterpulsation in dogs. Am J Emerg Med
1984;2(2):123-128.
13. Babbs CF. Interposed abdominal compression CPR: a comprehensive evidence-based
review. Resuscitation 2003;59(1):71-82.
14. Ralston SH, Babbs CF, Niebauer MJ. Cardiopulmonary resuscitation with interposed
abdominal compression in dogs. Anesth Analg 1982;61(8):645-651.
15. Field JM, Hazinski MF, Sayre MR, et al. Part 1: executive summary: 2010 American
Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation 2010;122(suppl 3):S640-S656.
16. Hazinski MF, Nolan JP, Billi JE, et al. 2010 international consensus on cardiopulmonary
resuscitation and emergency care science with treatment recommendations. Resuscitation 2010;81(1; suppl 1):e1–e332.
17. Barton L, Crowe DT. Open chest cardiopulmonary resuscitation. In: Bonagura JD, ed.
Kirk’s Current Veterinary Therapy XIII. Philadelphia: WB Saunders; 2000:147-149.
18. Feneley MP, Maier GW, Kern KB, et al. Influence of compression rate on initial success
of resuscitation and 24 hour survival after prolonged manual cardiopulmonary resuscitation
in dogs. Circulation 1988;77(1):240-250.
19. Yannopoulos D, Aufderheide TP. Use of the impedance threshold device (ITD).
Resuscitation 2007;75(1):192-193.
20. Emmerman CL, Pinchak AC, Hancock D, et al. Effect of injection site on circulation
times during cardiac arrest. Crit Care Med 1988;16(11):1138-1141.
21. Cole S, Otto C, Hughes D. Cardiopulmonary cerebral resuscitation in small animals:
a clinical practice review. J Vet Emerg Crit Care 2003;13(1):13-23.
22. Sabin HI, Coghill SB, Khunti K, McNeill CO. Accuracy of intracardiac injections
determined by a post-mortem study. Lancet 1983;2(8358):1054-1055.
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23. Jespersen HF, Granborg J, Hansen U, et al. Feasibility of intracardiac injection of
drugs during cardiac arrest. Eur Heart J 1990;11(3):269-274.
24. Rush JE, Wingfield WE. Recognition and frequency of dysrhythmias during cardiopulmonary arrest. JAVMA 1992;200(12):1932-1937.
25. Schmittinger CA, Astner S, Astner L, et al. Cardiopulmonary resuscitation with vasopressin in a dog. Vet Anaesth Analg 2005;32(2):112-114.
26. Bright JM, Wright BD. Successful biphasic transthoracic defibrillation of a dog with
prolonged refractory ventricular fibrillation. J Vet Emerg Crit Care 2009;193:275-279.
27. Dani C, Bertini G, Pezzati M, et al. Brain hemodynamic effects of doxapram in
preterm infants. Biol Neonate 2006;89(2):69-74.
28. van Pelt DR, Wingfield WE. Controversial issues in drug treatment during cardiopulmonary resuscitation. JAVMA 1992;200:1938-1944.
29. Callaham M, Barton C. Prediction of outcome of cardiopulmonary resuscitation from
end-tidal carbon dioxide concentration. Crit Care Med 1990;18(4):358-362.
Vetlearn.com | April 2011 | Veterinary Technician
30. Nozari A, Safar P, Stezoski SW, et al. Mild hypothermia during prolonged cardiopulmonary cerebral resuscitation increases conscious survival in dogs. Crit Care Med
2004;32(10):2110-2116.
31. Steingrub JS, Mundt DJ. Blood glucose and neurological outcome with global brain
ischemia. Crit Care Med 1996;24(5):802-806.
32. Kass PH, Haskins SC. Survival following cardiopulmonary resuscitation in dogs and
cats. J Vet Emerg Crit Care 1992;2(2):57-65.
33. Wingfield WE, van Pelt DR. Respiratory and cardiopulmonary arrest in dogs and
cats: 265 cases (1986-1991). JAVMA 1992;200(12):1993-1996.
34. de Vos R, Koster RW, de Haan RJ, et al. In-hospital cardiopulmonary resuscitation:
prearrest morbidity and outcome. Arch Intern Med 1999;159(8):845-850.
35. Waldrop JE, Rozanski EA, Swanke ED, et al. Causes of cardiopulmonary arrest,
resuscitation management, and functional outcome in dogs and cats surviving cardiopulmonary arrest. J Vet Emerg Crit Care 2004;14(1):22-29.
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Managing Cardiopulmonary Arrest
1 CE Credit
The article you have read qualifies for 1.0 credit hour. To receive credit from Alfred State College, choose the best answer to each of
the following questions. CE tests must be taken online at Vetlearn.com; test results and CE certificates are available immediately.
1. Ventilatory rates of _________ breaths/min are currently
recommended for veterinary patients in CPA.
a. 4 to 12
b. 10 to 24
c. 30 to 45
d. 60 to 82
2. Clinical signs of impending CPA include
a. a strong pulse.
b. audible heart sounds.
c. fixed, dilated pupils.
d. significant hypertension.
3. Which of the following is routinely recommended during
CPCR?
c. Patients that experience CPA and have CPCR withheld
show no increased morbidity compared with patients that
receive immediate CPCR.
d. VF is the most common arrhythmia observed in veterinary
patients during CPA.
7. Mild ____________ after resuscitation has been shown to
improve outcomes in dogs after CPA.
a. hypotension
b. hypovolemia
c. hypoxia
d. hypothermia
8. End-tidal carbon dioxide measurements ____________
have been associated with higher survival rates during
CPA.
a. epinephrine
a. <15 cm Hg
b. calcium
b. >15 cm Hg
c. sodium bicarbonate
c. <15 mm Hg
d. doxapram
d. >15 mm Hg
4. The __________ vein typically yields well to catheterization
during CPA and provides the shortest transit time for drugs
to reach the heart.
a. jugular
b. cephalic
c. saphenous
a. femoral
5. During CPCR, external cardiac massage should be
performed at a rate of _________ compressions/min.
9. In patients with PEA,
a. P waves, QRS complexes, and T waves may be observed
on the ECG.
b. no clear P waves, QRS complexes, or T waves are
observed on the ECG.
c. a rare P wave may be observed on the ECG, but no clear
QRS complexes are seen.
d. none of the above
10. Treatment of VF involves immediate
a. 10 to 60
a. insulin administration.
b. 30 to 60
b. thoracentesis.
c. 60 to 120
c. IV catheterization.
a. 80 to 120
d. electrical defibrillation.
6. Which of the following statements regarding CPA is true?
a. Published data suggest that approximately 50% of
patients experiencing CPA survive for >1 week after CPCR.
b. Functional recovery has been reported in most animals
that survive CPA.
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©Copyright 2011 MediMedia Animal Health. This document is for internal purposes only. Reprinting or posting on an external website without written permission from MMAH is a violation of copyright laws.