CHAPTER 4 • Post–Cardiac Arrest Care 17

CHAPTER 4
POST–CARDIAC ARREST CARE
Manuel Boller, DrMedVet, MTR, DACVECC • Daniel J. Fletcher, PhD, DVM, DACVECC

KEY POINTS • Hemodynamic optimization measures after ROSC include

administration of intravenous fluids, pressors, inotropes, and
• The systemic response to ischemia and reperfusion, anoxic brain
blood products to reach a mean arterial pressure (MAP) of
injury, postresuscitation myocardial dysfunction, and persistent
80 mm Hg or higher, an ScvO2 of 70% or more, and a lactate of
precipitating pathologic conditions define post–cardiac arrest care
less than 2.5 mmol/L.
measures needed for each individual patient.
• Mild therapeutic hypothermia (32° to 34° C) for 24 to 48 hours is
• Immediate post–cardiac arrest care focuses on prevention of
recommended in patients that remain comatose after ROSC if
rearrest by ensuring optimal ventilation, oxygenation, and tissue
mechanical ventilation and advanced critical care capability is
perfusion, as well as identifying and correcting reversible causes
available.
of cardiopulmonary arrest.
• Additional neuroprotective strategies include permissive
• Hypoxemia and hyperoxemia early after return of spontaneous
hypothermia, slow rewarming (0.25° to 0.5° C/hr), osmotic
circulation (ROSC) should be prevented by controlled
therapy, and seizure prophylaxis.
reoxygenation with a target SaO2/SpO2 of 94% to 98% or a PaO2
of 80 to 100 mm Hg. • Critically ill survivors should be referred to veterinary critical care
centers for post–cardiac arrest care.
18 PART I  • KEY CRITICAL CARE CONCEPTS

Ahead of his time, the Russian resuscitation scientist and physician PCA treatment, even if delayed after ROSC, can influence outcome
Vladimir Negovsky stated in 1972 that “after the first step in resusci- dramatically. Recent human epidemiologic data suggest that the
tation when heart function and respiration have been restored, the improvement in outcomes achieved after IHCA over the past 10 years
second step in resuscitation arises—the more complicated problems in part is due to increased postresuscitation survival.8 PCA arrest care
of treating the after-effects of a general hypoxia.”1 Since then, post– is now considered the final essential link of a comprehensive treat-
cardiac arrest (PCA) care has been increasingly emphasized as a key ment strategy to optimize outcomes from CPA (Figure 4-2).
element of cardiopulmonary resuscitation (CPR). Current CPR There are two paradigms of care during the PCA phase. One aims
guidelines in both human and veterinary medicine devote entire at pathophysiologic processes that occur in the postresuscitation
sections to the care of those patients that achieved return of sponta- phase, namely (1) ischemia and reperfusion (IR) injury, (2) PCA
neous circulation (ROSC) after cardiopulmonary arrest (CPA).2-5 brain injury, (3) PCA myocardial dysfunction, and (4) persistent
The rationale behind this is twofold. First, epidemiologic studies in precipitating pathologic conditions (Figure 4-3). The other paradigm
people show that two thirds of in-hospital cardiac arrest (IHCA) of care responds to a shift in treatment prioritization as time after
patients who achieve stable ROSC do not survive to hospital dis- ROSC progresses. Immediately after ROSC, the focus is on preven-
charge.6 In veterinary medicine 85% of dogs or cats with ROSC are tion of recurrence of cardiac arrest and limitation of organ injury.
euthanized or die before hospital discharge (Figure 4-1).7 Thus Later care emphasizes treatment of the underlying disease processes,
optimization of PCA care has the potential to save many lives. prognostication, and rehabilitation.2
Second, new opportunities for delivering complex therapies are
now available. Foremost, clear evidence of the neuroprotective PROPAGATING SUSTAINED ROSC
potential of mild therapeutic hypothermia (MTH) boosted the field
of PCA care. The protective effect of cooling also demonstrated that The majority of dogs and cats that are initially successfully resusci-
tated die within the first few hours because of rearrest.9 The goal
immediately after ROSC is to sustain spontaneous circulation and
perfusion of vital organs, such as the brain and the myocardium,
Alive attenuating further injury and preventing rearrest. Although patient
monitoring options are limited during CPA (see Chapter 3), common
Arrest
100% monitoring such as noninvasive blood pressure measurement and
pulse oximetry provide useful information after ROSC. Identification
CPR of any reversible cause of CPA needs to be proactively pursued. If not
~
~ 65% lost already addressed during advanced life support (ALS), it is important
to assess for abnormalities in electrolytes, glucose, acid-base status,
35% ROSC hematocrit, arterial oxygenation, and ventilation soon after ROSC.
PCA care ~
~ 85% lost Abnormalities such as hypoxemia, severe anemia, hypotension, and
6% Hospital discharge hyperkalemia or hypocalcemia must be corrected aggressively. The
Time
incidence of rearrest rhythms has not been systematically reported
FIGURE 4-1 The epidemiology of veterinary CPR is characterized by two in veterinary patients, but in people, shockable and nonshockable
phases of patient losses. First, the two thirds of patients that do not reach
rhythms are equally prevalent, with ventricular fibrillation (VF) and
ROSC despite initiation of CPR. Second, the large majority of patients that
pulseless ventricular tachycardia (VT) identified in 15% and 29%,
do not survive to hospital discharge, despite initial ROSC. Thus patient
management during the PCA phase is as important as CPR to improve respectively.10 If VT persists, treatment with lidocaine (2 mg/kg intra-
outcomes. (Data from Hofmeister EH, Brainard BM, Egger CM, et al: venous [IV] bolus, followed by a 30 to 50 mcg/kg/min infusion) is
Prognostic indicators for dogs and cats with cardiopulmonary arrest recommended. Catecholamine administration may be necessary to
treated by cardiopulmonary cerebral resuscitation at a university teach- maintain vascular tone and adequate blood pressure. Positive inotro-
ing hospital, J Am Vet Med Assoc 235(1):50-57, 2009.) pic support can serve to attenuate postischemic left ventricular

FIGURE 4-2 The chain of survival for dogs and cats symbolizing the continuum of care required to suc-
cessfully manage CPA. (From Boller M, Boller EM, Oodegard S, et al: Small animal cardiopulmonary
resuscitation requires a continuum of care: proposal for a chain of survival for veterinary patients,
J Am Vet Med Assoc 240(5):540-554, 2012.)
 CHAPTER 4 • Post–Cardiac Arrest Care 19

Post-cardiac Arrest Syndrome

Systemic ischemia- Post-cardiac arrest Post-cardiac arrest Persistent precipitation

reperfusion response brain injury myocardial dysfunction pathology

• Infection (sepsis,
pneumonia)
• Upper airway obstruction
• Cardiovascular disease
• SIRS (cardiomyopathy)
Pathophysiology

• Impaired vasoregulation • Impaired cerebrovascular • Pulmonary disease

• Increased coagulation autoregulation • Right and left ventricular (CHF, ARDS)
• Adrenal suppression • Cerebral edema (limited) dysfunction (myocardial * Thromboembolic disease
• Postischemic stunning) (PTE)
• Impaired tissue oxygen
delivery and utilization neurodegeneration • CNS disease
• Impaired resistance to • Toxicological (overdose,
infection poisoning)
• Hypovolemia (hemorrhage,
dehydration)
• MODS
Clinical manifestations

• Ongoing tissue
• Delirium, stupor, coma
hypoxia-ischemia • Reduced cardiac output
• Seizures • Specific to cause
• Hypotension • Hypotension
• Myoclonus • Complicated by
• Pyrexia (fever) • Arrhythmias
• Cognitive dysfunction concomitant PCA
• Hyperglycemia • Ongoing tissue
• Cortical blindness syndrome
• Multiorgan failure hypoxia-ischemia
• Brain death
• Infection

• Early hemodynamic • Therapeutic hypothermia

Potential treatments

optimization • Early hemodynamic

• Intravenous fluids optimization • Disease-specific
• Early hemodynamic
• Vasopressors • Airway protection and optimization • Guided by patient
mechanical ventilation condition and
• Temperature control • Inotropes
• Seizure control concomitant PCA
• Glucose control • Therapeutic hypothermia syndrome
• Controlled reoxygenation
• Antibiotics for (SaO2 94% to 98%)
documented infection • Supportive care

FIGURE 4-3 Flowchart summarizing pathophysiology, clinical manifestations, and potential treatments for
the four major components of the post–cardiac arrest syndrome. ARDS, Acute respiratory distress syn-
drome; CHF, congestive heart failure; MODS, multiorgan dysfunction syndrome; PCA, Post–cardiac arrest;
PTE, pulmonary thromboembolism; SIRS, systemic inflammatory response syndrome. (Modified with
permission from Boller M, Boller EM, Oodegard S, et al: Small animal cardiopulmonary resuscitation
requires a continuum of care: proposal for a chain of survival for veterinary patients, J Am Vet Med
Assoc 240(5):540-554, 2012.)

systolic dysfunction.11,12 Ventilatory assistance is almost invariably disease” more than 40 years ago.1 The syndrome shares many char-
necessary during the immediate postresuscitation phase and needs acteristics with severe sepsis, specifically in regard to inflammation,
to be delivered by either manual or mechanical ventilation with a coagulation, and the endothelium.1,13-28 After observing neutrophil
target PaCO2 of 32 to 43 mm Hg in dogs and 26 to 36 mm Hg in and endothelial activation paired with high concentrations of circu-
cats. Once sustained ROSC has been achieved for the first 20 to 40 lating cytokines (tumor necrosis factor α [TNF-α], interleukin 6
minutes, the clinician’s attention can be directed toward attenuation [IL-6], IL-9, IL-10) in the postarrest phase in humans, Adrie et al
of the evolution of further organ injury that arises as a consequence coined the term sepsis-like syndrome to describe the phenotype of
of IR and to titrate supportive care to the needs of the patient. post–cardiac arrest abnormalities.29 Thus the PCA patient may have
characteristics that are similar to severe sepsis and multiorgan dys-
SYSTEMIC RESPONSE TO ISCHEMIA AND function syndrome. With that in mind, therapeutic considerations
REPERFUSION: SEPSIS-LIKE SYNDROME involving (1) early hemodynamic optimization, (2) glycemic control,
and (3) critical illness–related corticosteroid insufficiency (CIRCI)
ROSC after the global ischemic event of CPA leads to a whole-body are being examined in human medicine and have relevance to veteri-
IR syndrome that Negovsky characterized as “post-resuscitation nary PCA care. Naturally, treatment is highly individualized, each
20 PART I  • KEY CRITICAL CARE CONCEPTS

element of care being carefully titrated to the patient’s needs. This of low-dose hydrocortisone (1 mg/kg IV followed by either 1 mg/kg
titration is guided by monitoring—that is, by assessment and reas- IV q6h or an intravenous infusion of 0.15 mg/kg/hr) in dogs and cats
sessment of predefined treatment endpoints. with vasopressor-dependent shock after CPA, with or without docu-
mented CIRCI, may be considered.33
Hemodynamic Optimization
Early goal-directed therapy (EGDT) was studied by Rivers et al more POST–CARDIAC ARREST BRAIN INJURY
than 10 years ago as a strategy of hemodynamic optimization in
patients with severe sepsis and septic shock.30 EGDT uses an algo- In humans, cerebral dysfunction after cardiac arrest is the single
rithm in which single interventions are started or discontinued based greatest concern and the most common single cause of death. In one
on the achievement of predefined physiologic endpoints with an study neurologic injury was the cause of death in two thirds of
emphasis on early resuscitation. In human medicine, the EGDT patients after out-of-hospital cardiac arrest (OHCA) and one fifth
approach has been implemented for PCA care as an early hemody- after IHCA.51 In small animals, PCA brain injury has been described
namic optimization protocol bundled together with mild therapeutic in experimental and clinical reports, but little is known about its
hypothermia.31,32 Included interventions are those to optimize tissue epidemiology.52-55 PCA brain injury results from global cerebral IR.56
oxygen delivery (fluid administration, vasopressors/inotropes, red Although the process is complex and not understood in its entirety,
blood cell transfusion, oxygen supplementation) and to decrease some aspects of cerebral IR injury are clear:
tissue oxygen demand (sedation, mechanical ventilation, neuromus- 1. Most of the injury is sustained during reperfusion and not during
cular blockade, temperature control). A veterinary PCA hemody- ischemia, affording the clinician the opportunity to intervene after
namic optimization algorithm has been published by the RECOVER ROSC is achieved.
initiative.33 Resuscitation endpoints are central venous pressure 2. Cytosolic and mitochondrial calcium overload leads to activation
(CVP; 0 mm Hg < CVP < 10 mm Hg), mean arterial blood pressure of proteases that may lead to neuronal death and production of
(MAP 80 to 120 mm Hg), and perfusion parameters (central venous reactive oxygen species (ROS).57,58
oxygen saturation [ScvO2] > 70 %; lactate < 2.5 mmol/L). Markers of 3. A burst of ROS occurs during reperfusion, leading to oxidative
vasodilation, such as injected mucous membranes or shortened capil- alterations of lipids, proteins, and nucleic acids propagating injury
lary refill time, pulse quality, and echocardiographic determination of neuronal cell components and limiting the cells’ protective and
of left ventricular function should also be included in a comprehen- repair mechanisms.56
sive hemodynamic assessment. Such monitoring will guide effective 4. Mild therapeutic hypothermia administered after ROSC is proven
yet safe treatment with fluids, vasopressors, and inotropes (see Chap- to reduce postresuscitation cerebral dysfunction.59
ters 8 and 183). Although there are no veterinary studies validating
this approach yet, goal-directed therapy is an excellent example for Brain Injury Sustained During Ischemia
how monitoring interacts with treatment. There is considerable Versus During Reperfusion
diversity of the PCA patient response to injury and treatment, and a Much of the injury sustained after CPA evolves during reperfu-
“one-size-fits-all” therapeutic strategy is not appropriate. sion rather than ischemia. By optimizing the reperfusion process,
extended durations of ischemia can be tolerated.60,61 Nevertheless, IR
Glycemic Control is a continuum that is initiated during cellular ischemia. A sudden
Hyperglycemia commonly occurs after cardiac arrest in humans and decline in oxygen delivery occurs upon onset of CPA. Glycolysis
has been associated with worse outcome.34-37 Mild to moderate allows for limited continued energy production, but cerebral adenos-
hyperglycemia combined with a total plasma insulin decrease of 60% ine triphosphate (ATP) stores are depleted within 2 to 4 minutes. In
was observed in experimental research in dogs early after ROSC.38 contrast, 20 to 40 minutes are required for the same to occur in the
Animal studies (including canine) have demonstrated that hypergly- intestines and the myocardium.62-64 Once ATP is depleted, cellular
cemia worsens ischemic brain injury.39-42 In humans, iatrogenic membrane potentials are rapidly lost. Clinically, any cardiac electrical
hypoglycemia occurred in 18% of PCA patients treated with tight activity as detected by electrocardiogram (ECG) provides evidence
glycemic control (4.4 to 6.1 mmol/L; 80 to 110 mg/dl). There is no that the global myocardial membrane potential has not yet subsided,
evidence that tight glucose control provides additional benefits over or, during reperfusion, has been reestablished once again. Large
a less stringent target, and moderate glycemic control targeting amounts of sodium, chloride, and calcium enter the cells, followed
glucose levels less than 180 mg/dl is currently suggested for human by cell swelling and membrane disruption. It is believed that the
PCA patients.3,36,43 A similar strategy in dogs and cats after cardiac combined influences of increased exposure to calcium, oxidative
arrest may be considered. Implementation of glycemic control with stress, and energy depletion lead to mitochondrial injury, finally
intravenous insulin administration follows the recommendation for leading to more ROS production upon reperfusion and to apoptosis
patients with severe sepsis (see Chapter 6). and necrosis.56,65 Therefore, controlled reperfusion strategies include
mild hypocalcemia and avoidance of hyperoxemia.57,61,66 Recent
Adrenal Dysfunction experimental studies have demonstrated neurologically intact sur-
Steroids are essential to the physiologic response to severe stress vival using these strategies even after 30 minutes of warm cerebral
and are important for the regulation of vascular tone and endo- ischemia.67,68
thelial permeability. CIRCI, or relative adrenal insufficiency (RAI),
after ROSC was identified in several human clinical studies and has Controlled Reoxygenation
been associated with increased mortality.44-49 Low-dose steroid Large amounts of ROS are generated after CPR.69-71 Becker and
administration for septic shock remains controversial,50 and direct Neumar summarized in detail the pathobiology of ROS because of
evidence supporting corticosteroid administration during PCA care IR in the PCA period.72,73 Excessive production of ROS in the pres-
is lacking. Because of this and the risk for infection, peptic ulcer, and ence of exhausted protective mechanisms peaks in elaboration of
exacerbation of postischemic neurologic injury associated with cor- highly reactive free radicals, namely hydroxyl radicals (•OH) and
ticosteroid administration, routine administration of corticosteroids peroxynitrite (ONOO•), which in turn cause cell membrane damage,
during PCA care is not recommended.33 However, administration lipid peroxidation, DNA damage, and protein alterations.
 CHAPTER 4 • Post–Cardiac Arrest Care 21

Rapid reoxygenation following prolonged global ischemia is an the entire potential of MTH will not be realized with this approach,
implied goal of CPR and essential for saving lives from cardiac arrest. it may attenuate the harmful effects of a rapid increase in brain
However, the absolute requirement of reintroducing oxygen conflicts temperature after ischemia. It is reasonable to target a rewarming rate
with the toxic potential of oxygen as substrate for ROS. of 0.25° C to 0.5°C (0.45° to 0.9° F) per hour.33 In addition, it is
Much evidence suggests that arterial hyperoxemia soon after important to prevent fever or hyperthermia after CPA because it is
ROSC increases oxidative brain injury, increases neurodegeneration, associated with increased mortality.3,37
worsens functional neurologic outcome, and negatively affects overall
survival.72 Retrospective clinical studies in humans demonstrated an Other Neuroprotective Treatment Strategies
association between post-ROSC hyperoxemia and in-hospital mor- Although epidemiologic data are lacking, clinical experience suggests
tality and documented a linear relationship between the degree of that post-CPA seizures can occur in dogs and cats. In humans, the
hyperoxemia and nonsurvival.74,75 In a canine experimental study, occurrence of seizures during the first 3 days after CPA is associated
titration of oxygen supplementation to an SpO2 of 94% to 96% with worse outcome. Nonconvulsive status epilepticus (i.e., only
compared with a consistent FiO2 of 1 lead to superior functional identified by electroencephalography) occurs commonly in humans
neurologic outcomes and a reduction in neuronal degeneration in who remain comatose after ROSC.85 Seizure activity leads to a drastic
vulnerable brain regions.55 The inspired oxygen concentration, espe- increase in cerebral metabolism and oxygen demand, possibly out-
cially early after ROSC, should therefore be titrated to normoxemia stripping oxygen supply. Thus patients should be monitored for sei-
(PaO2 80 to 100 mm Hg; SpO2 94% to 98%), avoiding both hypox- zures and treated accordingly if they occur (see Chapter 82).
emia and hyperoxemia.33 Prophylactic administration of barbiturates should also be consid-
ered.33 This may be particularly relevant in animals that remain
Mild Therapeutic Hypothermia comatose or are sedated, because nonconvulsive seizure activity may
Mild therapeutic hypothermia (MTH) is the only treatment proven be present and difficult to diagnose.
in clinical trials to be effective in increasing neurologically intact Cytotoxic and vasogenic cerebral edema have been described after
survival after resuscitation from OHCA, whereas conclusive data are CPA and are associated with poor neurologic outcome in people.86
still awaited for IHCA.3,76,77 MTH exerts its protective effects via a In contrast, intracranial hypertension (ICH) does not commonly
number of processes, including a reduction of mitochondrial injury occur,87 but if it does it can compromise cerebral perfusion pressure
and dysfunction, decrease in cerebral metabolism, reduction of and thus cerebral blood flow. In dogs, hypertonic fluid administra-
calcium inflow into cells and neuronal excitotoxicity, reduced pro- tion after 14 minutes of anoxic brain injury decreased cerebral edema
duction of ROS and reduced apoptosis, and suppression of seizure but did not affect survival or functional neurologic outcome.88 In
activity.59 MTH consists of reduction of the core body temperature general, the use of hypertonic solutions such as mannitol or hyper-
to 32° to 34°C (89.6° to 93.2° F). A variety of cooling methods have tonic saline for reduction of cerebral edema after cardiac arrest has
been used in humans, including cooling blankets, simple icepacks, not been well examined, and the few studies available demonstrate
intravenous infusion of ice cold saline, and endovascular cooling neither benefit nor harm.5 Thus the use of mannitol or hypertonic
devices.78 Cooling to target temperature early after ROSC, or even saline can be considered if the presence of cerebral edema is sug-
during reperfusion, is likely more effective than a delay in cooling.79 gested by clinical signs, such as coma, stupor, or decerebrate posture.33
The optimal duration of MTH is unknown, and likely varies, with Unfortunately the clinical signs of ICH overlap with the neurologic
the more severely injured patients requiring a longer duration of deficits often seen after CPA.
cooling. MTH for 24 to 48 hours is recommended in dogs and cats Induction of supranormal cerebral perfusion pressure during the
that remain comatose after ROSC, followed by rewarming at a slow PCA phase has been demonstrated to be beneficial, indicating that a
rate of 0.25° to 0.5° C (0.45° to 0.9° F) per hour.33 Patient manage- clinically relevant increased intracranial pressure or resistance to
ment and monitoring efforts may be considerable during MTH and blood flow exists. In dogs after 12.5 minutes of untreated ventricular
are likely similar to that needed for mechanical ventilation. However, fibrillation, more than 50% of the brain remained below baseline
the use of hypothermia has been described in veterinary medicine blood flow 1 to 4 hours after resuscitation but not in animals with
indicating that implementation of MTH is feasible.80,81 Clinical appli- hypertensive hemodilution with a hematocrit of 20% and a mean
cation of MTH requires managing the side effects. Cooling induces arterial pressure of 140 mm Hg.89 Similar results were found in
increased muscle tone and shivering, which in return leads to other animal studies of optimized brain perfusion after prolonged
increased oxygen consumption, metabolic rate, and respiratory and cardiac arrest.68 In addition to an increased intracranial pressure,
heart rates and requires sedation, endotracheal intubation, and ven- perivascular edema, intravascular coagulation, and a loss of blood
tilation.82 Cooling without sedation may abolish the protective effect flow autoregulation may also be responsible for the beneficial
of MTH.59 Other physiologic disturbances can occur, including effect of supranormal cerebral perfusion pressures after prolonged
changes in metabolism, acid-base status, electrolytes, ECG, drug cardiac arrest.90-94 It is likely that these mechanisms are of less impor-
elimination, coagulation, and immune function, and the clinician tance during shorter durations of CPA and thus a less aggressive
should be familiar with those alterations when using PCA cooling.59 perfusion pressure goal may be sufficient in most clinical veterinary
However, adverse effects associated with PCA hypothermia in cases.33 Experimental evidence suggests that the CO2 responsiveness
humans with OHCA were found to be on par with normothermic of cerebral arteries is disturbed for the first several hours after pro-
care and did not affect mortality.83,84 Nevertheless, the side effects longed ischemia such that arterial vasodilation in response to
profile may be different in different species such as dogs and cats and increasing PaCO2 is abolished.95-97 In contrast, with shorter durations
after IHCA, where sepsis and coagulopathy is not uncommon. If of cerebral ischemia or later after reperfusion, CO2 responsiveness
either of these conditions is present, the benefit of MTH needs to be was maintained or restored such that hyperventilation after ROSC
carefully weighed against the risk. reduced cerebral blood flow and worsened neurologic outcomes
Many small animals are spontaneously hypothermic after CPA. compared with normoventilation.96,98-100 Similarly, the decreased
Allowing the patient to slowly rewarm to normal core temperature tissue pH associated with hypoventilation could be harmful.
over many hours after CPA without quick active rewarming (i.e., It is therefore reasonable to avoid both hypoventilation and
permissive hypothermia) offers an alternative to MTH. Even though hyperventilation after ROSC and to control ventilation such that
22 PART I  • KEY CRITICAL CARE CONCEPTS

normoventilation is achieved (dog: PaCO2 32 to 42 mm Hg; cat:

MYOCARDIAL DYSFUNCTION
PaCO2 26 to 36 mm Hg).33
Myocardial dysfunction (MD) is well described after cardiac arrest
Neurologic Assessment and Prognostication in experimental studies and in humans and has been the subject of
Assessing the patient’s PCA neurologic status is relevant for treat- one recent veterinary case report.12,14,111 MD occurs even in cases free
ment decisions and prognostication. Complete neurologic examina- of coronary artery disease and, like brain injury, its extent is attenu-
tions should be undertaken directly after ROSC and initially every 2 ated by hypothermia. PCA myocardial dysfunction is characterized
to 4 hours. Care should be taken to interpret the findings in light of by increased central venous and pulmonary capillary wedge pressure,
factors that confound the neurologic examination, such as sedation, reduced left- and right sided systolic and diastolic ventricular func-
neuromuscular blockade, seizures, and postictal status. Neurologic tion with increased end-diastolic and end-systolic volume, and
deficit scoring systems that include metrics of consciousness, motor reduced left ventricular ejection fraction and cardiac output.11,12,14,111,112
and sensory function, and behavior have been used in clinical and These changes may be further complicated by ventricular tachyar-
experimental studies using dogs.53,101 Alternatively, the Modified rhythmia, together leading to cardiogenic shock in severe cases. MD
Glasgow Coma Scale (MGCS), originally developed for dogs with is reversible and typically resolves within 48 hours.12,14 This revers-
traumatic brain injury, can be used to systematically assess and track ibility in the absence of cell necrosis is the basis for the term myocar-
the patient’s overall PCA neurologic status, although it has not been dial stunning. Mechanisms of injury are not fully understood and are
validated for this indication.102 The MGCS assesses function of the multifactorial. Myocyte dysfunction results from cellular processes
brainstem (cranial nerve reflexes) and cerebral hemispheres (motor associated with cellular IR comparable to those evolving in the
response) in conjunction with the level of consciousness. nervous system.113 Thus the severity of MD depends on the duration
In principle, any retention of normal neurologic function imme- and extent of myocardial ischemia as well as the conditions under
diately after ROSC supports a favorable prognosis. Conversely, which reperfusion occurs (e.g., presence or absence of hypothermia).
studies of comatose human survivors of CPA suggest that clinical Second, a lack of capillary blood flow during PCA (myocardial
neurologic examination is not a reliable predictor of poor outcome no-reflow) may occur.14,114 Microvascular obstruction or plugging
during the first 24 hours after ROSC.103 Early absence of pupillary may occur subsequent to endothelial cell activation and swelling,
light response (PLR) in comatose patients led to a false-positive rate neutrophil–endothelial cell interactions, activation of coagulation,
for prediction of irreversible unconsciousness of more than 30%.104 and platelet aggregation.114 Pericapillary edema will further impede
Between 24 and 72 hours, presence of coma and absence of PLR microvascular blood flow. With alterations in capillary permeability,
significantly increased the likelihood of poor neurologic outcomes, the subsequent increase in microvascular hematocrit and total
but conscious survival is possible. It is not until 3 days after ROSC protein and the associated rheologic properties, tissue blood flow
that lack of PLR and absence of motor response to a painful stimulus can be impaired. Moreover, postischemic red blood cells may have
predict reliably that a human patient will fail to regain conscious- reduced deformability and have a tendency toward endothelial cell
ness.103 Sedation and MTH will further delay the ability for definitive adhesion and to form erythrocyte plugs. Third, several factors were
prognostication.105 Even though no comparable data are available for found to worsen MD, including intra-arrest administration of epi-
veterinary patients, the notion that early clinical prognostication of nephrine and high energy and monophasic waveform defibrilla-
the final neurologic outcome is unreliable is likely true in dogs and tion.14 Diagnosis and monitoring of progression and resolution of
cats also. Apart from clinical neurologic examinations, other prog- MD during the PCA phase is best accomplished noninvasively via
nostic tools have been examined. Electrophysiologic measurements, serial echocardiography.12 However, therapeutic decision making
such as electroencephalography (EEG), somatosensory evoked demands additional monitoring of right-sided filling pressures, to
potentials (SSEP) and brainstem auditory evoked response (BAER), limit the risk for hydrostatic pulmonary edema, and of perfusion
were shown to aid in early detection of futility in humans.103 Depend- parameters (e.g., lactate, ScvO2). MTH attenuates MD.115-117 No other
ing on the available veterinary expertise, electrophysiologic assess- treatments have been identified to be clinically effective in attenuat-
ment may be useful in dogs and cats as an adjunct to neurologic ing the occurrence of PCA MD at this time.111 Dobutamine admin-
examination. BAER has been well described in the veterinary litera- istration at typical clinical doses used in dogs and cats was shown to
ture for auditory assessment, although reports on its use in ischemic effectively improve left ventricular function and cardiac output.
brain injury in dogs or cats are sparse.106,107 Elevations of neuron- Cardiac arrhythmias should be addressed commensurate to their
specific enolase (NSE) levels in cerebrospinal fluid (CSF) or plasma, significance (see the Cardiac Disorders section).
a commonly used biomarker of neuronal injury after CPA, were
found to imply poor neurologic outcome in experimental animal and PERSISTENT PRECIPITATING PATHOLOGY
clinical human studies, but the assay is not available for clinical vet-
erinary use at this time.103,108,109 Brain imaging modalities, such as IHCA, the most common CPA scenario confronting the small-animal
computed tomography or magnetic resonance imaging, are currently clinician, is often triggered by preexisting disease processes, such as
insufficiently validated for prediction of neurologic outcomes.103 severe sepsis, trauma, or respiratory failure. These pathologic condi-
Taken altogether, veterinary neurologic prognostication currently tions will likely persist after ROSC. They will affect the specific PCA
depends on clinical findings and in some instances BAER or EEG. care provided and influence the prognosis. Precipitating processes
Moreover, it is important to recognize that futility of care from a and preexisting comorbidities add great variability to the PCA patient
neurologic point of view is difficult to predict during the first 24 to population. Limited information is available about what these factors
72 hours. One clinical implication of this is that costly PCA care in are in small-animal patients. In one veterinary study including 204
animals that remain comatose after ROSC has to be initiated in the dogs and cats, causes of CPA were identified as hypoxemia (36%),
absence of valid neurologic prognostication. In addition, it is impor- shock (18%), anemia (13%), arrhythmia (8%), MODS (6%), trau-
tant to recognize that there is significant potential for neurologic matic brain injury (5%), anaphylaxis (1%), or other causes (21%).7
recovery, provided adequate supportive care is possible. Waldrop et al Another study suggests that trauma is a more common clinical
(2004) documented that neurologic abnormalities present after feature in cats compared with dogs with CPA.9 Meaney et al identi-
ROSC, such as dullness, ataxia, circling, seizures, and blindness, fied in 51,919 human patients with IHCA as cause of cardiac
resolved in 90% of CPA survivors before hospital discharge.110 arrest: hypotension (39%); acute respiratory failure (37%); acute
 CHAPTER 4 • Post–Cardiac Arrest Care 23

myocardial infarction (10%); and metabolic/electrolyte disturbances of outcome after successful cardiopulmonary resuscitation, Crit Care
(10%).118 In dogs, the first identified rhythm is by far more com- Med 31(3):805-811, 2003.
monly asystole and PEA than pulseless VT/VF.53 In humans, survival 17. Oppert M, Gleiter CH, Muller C, et al: Kinetics and characteristics of an
to hospital discharge after IHCA is markedly worse in patients with acute phase response following cardiac arrest, Intensive Care Med
25(12):1386-1394, 1999.
PEA/asystole compared with VT/VF.8,118-120 Because nonshockable
18. Negovsky VA: Postresuscitation disease, Crit Care Med 16(10):942-946,
rhythms do more commonly occur as a result of severe systemic 1988.
disease than VF/VT, this serves as indirect indicator of the impor- 19. Adrie C, Monchi M, Laurent I, et al: Coagulopathy after successful car-
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