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Cardiogenic Shock and Cardiac Arrest
CRITICAL CARE: CARDIOVASCULAR FOCUS
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CARDIOGENIC SHOCK AND CARDIAC ARREST Etienne Cote, DVM
CARDIOGENIC SHOCK
As cardiac disease of any type evolves, it usually passes through distinct stages. First is the asymptomatic stage, at which time there is no overt manifestation of heart disease, but medical evaluation can reveal an abnormality such as a murmur ausculted during physical examination or an arrhythmia detected on electrocardiography (ECG). Next, as progression continues, decompensation occurs. In this state, endogenous compensatory mechanisms that had sustained the asymptomatic state are overwhelmed by worsening heart disease, and perceptible abnormalities such as dyspnea or cough from pulmonary edema, syncope from an arrhythmia, or abdominal distention from cardiogenic ascites are apparent. If these abnormalities are not controlled with medication, surgery, or other therapy, further deterioration occurs and can lead to a life-threatening situation. At such an extreme, when a primary cardiac problem is responsible for inadequate systemic perfusion and the metabolic needs of the body's tissues are not met as a result of cardiac dysfunction, cardiogenic shock exists. 5' 9 Cardiogenic shock is a critical state that must be addressed urgently if the patient's life is to be saved. Causes of Cardiogenic Shock
The history of small animals that experience cardiogenic shock may or may not involve previously documented heart disease. When heart
From the Section of Cardiology, Angell Memorial Animal Hospital, Boston, Massachusetts
VETERINARY CLINICS OF NORTH AMERICA: SMALL ANIMAL PRACTICE VOLUME 31 • NUMBER 6 • NOVEMBER 2001
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disease has been documented previously, cardiogenic shock usually is the result of an acute exacerbation of the underlying problem such as rupture of a chorda tendinea or rupture of the wall of the left atrium in chronic mitral valvular disease, or severe pulmonary edema from acute ingestion of high-sodium foods or owner noncompliance with medications in cases of chronic valvular heart disease or cardiomyopathy. By contrast, when heart disease has not been diagnosed previously, a sudden onset of cardiogenic shock suggests a new, acute, or rapidly progressive cardiac problem such as acute idiopathic pericardia! effusion causing cardiac tamponade or represents a delay in seeking medical attention for a long-standing disorder. It is worth noting whether the patient in cardiogenic shock is already being treated for cardiac disease, because the treatment plan and prognosis are affected: adverse effects of medications, a more diseased heart, and fewer therapeutic options if refractory heart failure is present are more likely with advanced heart disease. In companion animals in which heart disease has been diagnosed previously, essentially any cardiac disorder, if severe enough, can lead to cardiogenic shock or cardiac arrest. The list of frequent newly diagnosed cardiac problems that are first detected when an animal is presented in cardiogenic shock is limited; cardiac tamponade from acute pericardia! effusion (idiopathic inflammatory, secondary to left atrial rupture, or malignant), chordae tendineae rupture, dilated cardiomyopathy, heartworm caval syndrome, and, occasionally, congenital malformations such as subaortic or pulmonic stenosis or end-stage patent ductus arteriosus are common in dogs, and cardiomyopathy with or without embolic disease, valvular heart disease, and, rarely, other congenital heart diseases are seen in cats. Cardiogenic Shock: Diagnosis
Cardiogenic shock is a state of severe circulatory compromise that is caused entirely by cardiac dysfunction. It is an extreme form of "forward" heart failure-the inability to generate a cardiac output sufficient to meet the body's demands. Clinical signs are referable to underperfusion of organs, particularly the brain (altered mentation consisting of disorientation, poor responsiveness, or unconsciousness), skeletal muscles (weakness, collapse), respiratory system (e.g., compensatory tachypnea due to metabolic acidosis), or heart itself (arrhythmias caused by decreased coronary circulation). An exception to this definition is a state of shock arising solely from a cardiac arrhythmia (i.e., when the heart is structurally normal). Severe hypotension caused by cardiac arrhythmia in an otherwise normal heart is classified not as cardiogenic shock but as cardiac arrest. Cardiogenic shock is confirmed when a patient has "poor cardiac output and evidence of tissue hypoxia in the presence of adequate intravascular volume." 5 In small animal medicine, such confirmation usually comes through noninvasive means, especially from the history
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and physical examination, thoracic radiography, ECG, indirect blood pressure measurement, and echocardiography. Rarely, cardiogenic shock is diagnosed in small animals as it is in human patients, in which the diagnostic criteria include (1) systemic arterial hypotension (mean <90 mm Hg for at least 1 hour and without response to intravenous fluids or a value 30 mm Hg below basal values for at least 30 minutes), (2) elevated arteriovenous oxygen difference (>5.5 mL/ dL), (3) depressed cardiac output (cardiac index <2.2 L/min/m2 body surface area) despite positive inotropic drugs, and (4) elevated pulmonary wedge pressure (>15 mm Hg). 5' 10 Physical examination of a patient in cardiogenic shock reveals an animal that on initial approach is usually either in overt distress (often showing disorientation, tachypnea, increased respiratory effort, and anxious expression) or is recumbent and poorly responsive or unresponsive. Poor perfusion is usually apparent from cool extremities and pale mucous membranes; the pulse is weak to absent as a result of poor cardiac output. Cardiac auscultation may be difficult if breath sounds are loud as a result of markedly increased respiratory effort or if pleural or pericardia! effusion is present to obscure the heart sounds. Nevertheless, a murmur or a gallop "rhythm," which is a third heart sound heard best with the bell of the stethoscope rather than the diaphragm, may be heard. This suggests increased left ventricular filling pressure and supports the suspicion of decompensated heart disease. The apex beat, or palpable heartbeat on the chest, may be diminished or absent such as in cardiac tamponade or dilated cardiomyopathy, or it may be vigorous if a large part of the left ventricle's volume is failing to reach the systemic circulation as in extreme mitral regurgitation. A vigorous apex beat in an animal with cool extremities or poor pulse quality should also prompt the consideration of noncardiac forms of shock such as hypovolemic or septic shock, requiring evaluation and treatment different from those of cardiogenic shock. Thoracic radiography is an essential part of the minimum database in a patient with cardiogenic shock. The major exception involves delaying radiography in favor of emergency treatment if obtaining the radiograph is thought to pose an immediate risk to the patient. Thoracic radiographs of a patient in cardiogenic shock answer at least two important questions: • Are there radiographic changes that support the suspicion of underlying cardiac disease? Common changes include an enlarged cardiac silhouette, atrial enlargement, and pulmonary venous and caudal vena caval engorgement. • Is there evidence of decompensation (i.e., congestive heart failure [CHF])? Such signs include pulmonary edema (left-sided CHF) and pleural effusion (left- or right-sided CHF). The clinician should be aware that the extent of cardiomegaly may be mildly attenuated by hypovolemia and possibly by tachycardia. 21 Many combinations of findings are commonly encountered. Examples
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include a large cardiac silhouette without left atrial enlargement but with small pulmonary vessels and a large caudal vena cava, which is a combination typical of pericardia! effusion; pleural effusion, pulmonary edema, and a mildly to markedly enlarged cardiac silhouette, which are frequently observed with decompensated feline heart diseases of many types; and cardiomegaly with left atrial enlargement, pulmonary venous congestion, and pulmonary edema in chronic mitral valve disease or dilated cardiomyopathy. ECG most commonly demonstrates sinus tachycardia, which is usually "appropriate"-it typically is baroreflex mediated, or aimed at increasing cardiac output in the face of critical hypotension. To deliberately suppress such a tachycardia is contraindicated, because this would likely decrease cardiac output and further exacerbate shock. Supraventricular tachycardias are actively suppressed (e.g., with intravenous propranolol or diltiazem) only when they are confirmed by a cardiologist to be self-perpetuating rhythms such as the Wolff-Parkinson-White syndrome (rare) or when they are so extreme (e.g., sustained heart rate >220-280 beats per minute in a giant- or small-breed dog, respectively, or >340 beats per minute in a cat) that adequate diastolic filling of the ventricles essentially cannot occur and the tachycardia itself contributes to the state of shock. The fine line between appropriate and excessive tachycardia is different for every patient, and suppression of an appropriate sinus tachycardia can cause cardiac arrest. Most supraventricular tachycardias in cardiogenic shock are appropriate and are best addressed with treatment of the underlying problem and concurrent issues such as hypotension, hypoxia, and acid-base or electrolyte disturbances rather than pharmacologic manipulation of the heart rate. If in doubt, the clinician can first perform a carotid sinus massage to attempt to suppress the heart rate and should note whether a more normal rate is sustained and whether pulse quality improves. Ventricular arrhythmias are also common during cardiogenic shock. Intermittent ventricular premature complexes may reflect myocardial hypoxia or similar insult and are generally not treated with antiarrhythmics. A sustained ventricular arrhythmia with hypotension and poor perfusion fulfills the criteria for cardiogenic shock or cardiac arrest, however, and is treated accordingly. As with any patient with ventricular arrhythmias, management of the patient in cardiogenic shock must involve identification and correction of any underlying problems that could precipitate the arrhythmia and make it refractory to treatment. Such problems include hypokalemia, acid-base disorders, hypoxia, disseminated intravascular coagulation, and marked anemia. Bradycardia may be the cause of cardiogenic shock or cardiac arrest, as in third-degree heart block with a slow ventricular rate, or it may be a sign of deteriorating cardiogenic shock and imminent cardiac arrest as is usually seen when a tachycardia suddenly converts to a severe bradycardia. 16 Bradycardia during cardiogenic shock should be treated with atropine (0.02-0.04 mg/kg intravenously). If this is ineffective, isoproterenol may be administered at a rate of 0.04 to 0.08 J.Lg/kg/min as a continuous rate infusion (CRI) with the dose adjusted based on
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response so as to avoid tachycardia. If the bradycardia continues to be unresponsive and the cardiogenic shock state persists, cardiac pacing may be indicated. If respirations have ceased, cardiopulmonary resuscitation (CPR) is warranted. Arterial blood pressure measurement is a cornerstone of the diagnosis and management of cardiogenic shock. The most common widely used measurement technique is Doppler ultrasonography with sphygmomanometry, which provides measurements of systolic pressure in most dogs and cats. 2• 20 In the clinical setting, the monitoring of blood pressure in a patient in cardiogenic shock must be performed continuously or as frequently as is possible without detracting from the patient's other needs (e.g., oxygen cage). Unfortunately, many criteria that could be extrapolated from human critical care medicine rely on diastolic or mean blood pressures, which are difficult or impossible to obtain by Doppler techniques. Oscillometric blood pressure evaluation measures these parameters, but results of experiments comparing this technique with direct measurement by arterial puncture have been mixed. 2• 3• 13• 20 Echocardiography greatly helps to pinpoint the lesion causing cardiogenic shock. As for any cardiac patient, the echocardiogram is often excellent at revealing the exact cardiac lesion, but fairly poor at showing the impact of that lesion on the patient. For example, echocardiography is useless for the diagnosis of pulmonary edema. In an animal in cardiagenic shock (excluding critical hypotension caused by severe arrhythmia defined previously as cardiac arrest rather than shock), echocardiography invariably reveals substantial structural heart disease. An animal suspected of having cardiogenic shock whose echocardiogram and thoracic radiographs are within normal limits probably does not have cardiogenic shock; other types of shock such as hypovolemic, distributive, or septic shock should be considered. It is common for dogs or cats with advanced cardiac disease to be treated with drugs that deplete intravascular volume, particularly diuretics. If such drugs are given in excess, or in normal doses but with decreased food or water intake, hypovolemia can occur. Hypovolemic shock induced by diuretic excess in cardiac patients is a fairly common clinical entity. When acute, this situation may be mistaken for cardiagenic shock, because such a patient may be showing signs of poor perfusion, be demonstrably hypotensive, and have physical signs of heart disease such as a heart murmur. It is important to differentiate cardiogenic shock from diuretic-induced hypovolemic shock of cardiac patients, because treatment of the former revolves around improving cardiac output, whereas treatment of the latter is based on judiciously restoring intravascular volume with intravenous fluids and close monitoring to detect recurrence of congestion (Table 1). Cardiogenic Shock: Treatment
Treatment of cardiogenic shock has one goal-to support the circulation until definitive improvement of cardiac function can be achieved.
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~ Table 1. CLINICAL FEATURES OF CARDIOGENIC SHOCK VERSUS CHRONICALLY TREATED HEART DISEASE WITH ACUTE HYPOVOLEMIA* Cardiogenic Shock
History
Dyspnea, disorientation
Medication history
Not previously stabilized with or receiving a long-term course of cardiac medications (e.g., diuretics, digoxin, or angiotensin-converting enzyme inhibitors)
Physical examination
Thoracic radiographs
Pleural effusion or pulmonary edema
Clinical pathologic findings
Complete blood cell count/chemistry/U-A often unremarkable, respiratory alkalosis or acidosis with hypoxemia and desaturation common (pulmonary edema)
Arterial blood pressure Electrocardiogram
Low (<90 mm Hg mean)
Echocardiogram
Usually tachycardia; acute transition from tachycardia to bradycardia means cardiac arrest likely imminent
Common to Both
Anorexia, lethargy, weakness, collapse
Heart Disease and Hypovolemia
Vomiting Almost invariably receiving long-term cardiac medications (especially diuretics but also digoxin, angiotensin-converting enzyme inhibitors)
Lethargy ± collapse, tachypnea, tachycardia, poor pulse quality; murmur, gallop, arrhythmia may be present or absent Cardiomegaly
Sinus tachycardia; ventricular and supraventricular tachyarrhythmias Moderate to marked structural heart disease
Tacky/ dry mucous membranes, halitosis
Microcardia is rare because of predominant heart disease-induced cardiomegaly Azotemia and isosthenuria (diuretics ± primary renal), hemoconcentration (increased albumin and globulin, packed cell volume may be normal if hemoconcentraton and anemia of chronic disease occur jointly), metabolic acidosis Normal to low Usually tachycardia
'Some patients in a category may not show all the characteristics listed for that category. It is also worth noting that these two categories are not mutually exclusive, and that animals with deteriorating heart disease may have features of hypovolemia and cardiogenic shock.
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In human medicine, long-standing improvement often is successfully achieved with definitive correction of the underlying heart disorder, including revascularization of the heart in coronary artery disease, surgical replacement of defective heart valves, resection or ablation of interventricular septal hypertrophy in hypertrophic cardiomyopathy, and cardiac transplantation. Because such long-term solutions exist, treatment of cardiogenic shock in human beings can be aimed at direct temporary relief of the inciting cause (e.g., medical dissolution of a thrombus causing myocardial infarction) and can legitimately involve sophisticated temporary techniques such as intra-aortic balloon pump implantation and left ventricular assist devices as "bridges" to a permanent solution. The technical, physical (patient size), and financial limitations of veterinary medicine are keenly apparent in the treatment of cardiogenic shock. First, there are few proven definitive corrections of underlying heart disease for which to strive in an animal with cardiogenic shock. Specific examples that do exist include relief of cardiac tamponade through pericardiocentesis, balloon pericardiotomy, or pericardiectomy; surgical removal of heartworms; and ligation or occlusion of a longstanding patent ductus arteriosus. Unfortunately, these conditions make up only a small proportion of cases of cardiogenic shock. In the absence of an intervention that can reverse the underlying cardiac problem in the long term, treatment of cardiogenic shock in animals aims to stop hemodynamic collapse in the hope that chronic medical management of heart disease can then increase longevity and quality of life. This approach has two inherent drawbacks that the clinician must recognize: the long-term benefits are not as good in the absence of definitive correction, and the prognosis probably worsens with each new occurrence of decompensation as the underlying process worsens. The primary goals of treatment are as follows: • To maintain oxygen delivery to the organs through adequate circulation • To avoid negative effects during such treatments Initial Approach To Treatment
All treatment of cardiogenic shock should involve an initial search for underlying problems that contribute to the shock state or may potentially complicate treatment (Table 2). Furthermore, because neither the natural evolution of cardiogenic shock nor the response to treatment can be predicted in a given case, ongoing monitoring during treatment is important. Monitoring techniques are essentially the same techniques as those described for the diagnosis of cardiogenic shock. In a successfully treated patient, physical examination reveals improved mentation, normalization of respiratory rate and effort, and evidence of improved peripheral perfusion such as warmer extremities and improved pulse
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Table 2. FACTORS THAT CONTRIBUTE TO OR COMPLICATE CARDIOGENIC SHOCK Factor
Hypoxia
Test
Anemia
Pulse oximetry, arterial blood gas Blood gas Serum electrolyte determination Packed cell volume
Hypoalbuminemia
Serum albumin
Pleural effusion Pericardia! effusion
Radiograph Echocardiogram
Acid-base imbalance Electrolyte imbalance
Treatment
Oxygen supplementation, improved diffusion (e.g., if edema) or improved ventilation Based on type of imbalance Appropriate intravenous crystalloid Transfusion of packed red blood cells, whole blood, or polymerized hemoglobin; control of hemorrhage if applicable Plasma transfusion, or other intravenous colloids Thoracentesis Pericardiocentesis
quality. Thoracic radiographs should demonstrate resolution of pulmonary edema if it is present, although a radiographic lag time of up to 24 hours between overt clinical improvement and radiographic improvement can occur. Arterial blood pressure should normalize, and additional hemodynamic parameters are evaluated if possible. Specifically, central venous pressure reflects the preload on the right heart and should decrease into the normal range ( <10 mm Hg) with control of right heart failure. Pulmonary capillary wedge pressure (PCWP) is obtained with a pulmonary arterial (Swan-Ganz type) catheter. The PCWP catheter is passed percutaneously into the jugular vein; under either fluoroscopic or pressure waveform guidance, it is then directed into the pulmonary artery. This procedure may be particularly challenging in smaller animals or animals with tricuspid regurgitation. Once in place, however, the catheter allows serial wedge pressure measurements to be obtained during treatment (normal range of mean PCWP: 8-14 mm Hg). Because it reflects left atrial pressure, PCWP is an invaluable tool to guide intravenous fluid administration and vasoactive drug use in patients with heart disease. A mean PCWP greater than 15 mm Hg suggests an excessive pressure load in the pulmonary venous circulation and risk of pulmonary edema; ongoing treatment to reduce PCWP is indicated. Conversely, a low or low-normal PCWP in a patient with cardiogenic shock suggests overcorrection such as occurs with excess diuretics or misdiagnosis such as occurs with noncardiogenic pulmonary edema. Reassessment of the treatment plan and intravenous fluid administration are essential when PCWP is low during management of cardiogenic shock Treatment of Specific Clinical Entities in Cardiogenic Shock
Simultaneous Hypotension and Pulmonary Edema. This situation is one of the hallmarks of cardiogenic shock, reflecting decreased cardiac
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output and high left atrial pressure. Clearly, a therapeutic challenge exists, because the treatment of either abnormality can worsen the other: use of diuretics to reduce pulmonary edema further depletes intravascular volume and worsens hypotension, and intravenous crystalloid infusion or vasopressor therapy increases left heart and pulmonary venous pressures and thus increases the tendency for pulmonary edema formation. Oxygen therapy should be administered in all cases. Cardiogenic pulmonary edema should be confirmed as the sole cause for the clinical and radiographic pulmonary abnormality. Noncardiogenic pulmonary edema, or acute respiratory distress syndrome, and pulmonary hemorrhage can be mistaken radiographically for the interstitial infiltrate of cardiogenic pulmonary edema. Hemodynamic monitoring is ideal for confirming or refuting a cardiogenic cause for pulmonary edema; less optimal is evaluation of the response to diuretic therapy in the face of confirmed structural heart disease. Analysis of pulmonary secretions if expectorated or if the animal is intubated is also useful; cardiogenic edema fluid should have a total protein content lower than that of plasmaP• It is essential to address predisposing factors that could be contributing either to edema. formation or hypotension. Moderate to marked hypoalbuminemia greatly increases the tendency for pulmonary edema formation, 8 " and correction with plasma transfusion or synthetic colloids is warranted. Severe bradycardia, usually with concurrent chronic mitral valve disease, can cause pulmonary edema and arterial hypotension. Bradycardia in the face of systemic hypotension and pulmonary edema is grossly abnormal, because baroreceptor and neurohormonal mechanisms should elicit a reflex tachycardia. As a result, treatment is usually required. A positive chronotrope such as atropine (0.02-0.04 mg/kg administered intravenously) or glycopyrrolate (0.1 mg/kg administered intravenously) should be used first. If these drugs are ineffective, cardiac pacing is indicated. Increasing the heart rate to the normal range raises the cardiac output, which increases systemic arterial pressure and, barring severe structural heart disease such as marked mitral valve regurgitation, lowers left atrial pressure. Pulmonary edema and hypotension can be improved by correcting cardiac dysfunction. Unfortunately, therapeutic options remain limited and unproved. Systolic dysfunction is treated with positive inotropes such as dobutamine, although diastolic dysfunction has no effective emergent treatment. If improving cardiac function is ineffective or impossible, the more severe abnormality (pulmonary edema vs hypotension) should be treated first. Typically, this is pulmonary edema, which is treated with furosemide (2-8 mg/kg intravenously every 2-8 hours as needed). Clearly, the concurrent risk is worsening hypovolemia, with hypoperfusion of vital organs, and adjunctive measures such as the application of medical antishock trousers 12" or an equivalent external wrap may be considered (although these measures are rarely used in this setting). The use of vasodilators for managing pulmonary edema is
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relatively contraindicated in the presence of hypotension. In normotensive or mildly hypotensive patients, however, they may be used alone or in conjunction with positive inotropes. Examples of vasodilators include nitroglycerin, hydralazine, angiotensin-converting enzyme inhibitors such as enalapril, and sodium nitroprusside (see article on cardiovascular pharmacotherapy in this issue for further details). When life-threatening pulmonary edema exists in the presence of severe myocardial dysfunction, dobutamine can be used together with a potent vasodilator such as hydralazine or sodium nitroprusside. Drugs that increase arterial pressure through arterioconstriction such as phenylephrine or dopamine may be used in conjunction with measures that increase cardiac performance such as dobutamine in cases of systolic failure and severe hypotension. Because these vasopressors impose an increase in afterload on an already failing heart, using them alone (without the addition of a positive inotrope) may further exacerbate pulmonary edema. Optimal treatment is aimed at correction of the underlying cause, but unlike the case in human beings, definitive correction of hypertrophic or dilated cardiomyopathy with heart transplantation, subaortic stenosis with open-heart myotomy or myectomy, or valvular heart disease with valve repair or replacement is either impractical or simply not performed in veterinary patients. Decreased Contractility and Cardiogenic Shock. The simple solution for systolic dysfunction, or decreased contractility, of the left ventricle in the setting of cardiogenic shock is to administer drugs that increase contractility, namely, positive inotropes such as dobutamine (2-20 J..Lg/ kg/min administered intravenously as a CRI) (Table 3).* (Regrettably, these drugs also simultaneously increase myocardial oxygen demand, which predisposes to potentially malignant arrhythmias and may lead to long-term detriment.) Clinical trials of dobutamine infusion in patients with severe CHF remain divided in their findings: most show hemodynamic improvement with dobutamine (short-term benefit) but not an increase in survival (equivocal or negative long-term effect). 15• 19 The applicability of these findings to veterinary patients is unclear; the rarity of myocardial infarction in small animals may mean that patients generally have a greater amount of myocardium to respond to inotropes (beneficial), although, conversely, the absence of long-term corrections of primary heart problems may signify that the overall longevity or quality of life is not improved appreciably with inotrope infusion. In the absence of definitive guidelines, an intuitive but unproved recommendation is to begin with infusion of a low dose of an inotrope, titrate the intravenous CRI upward gradually until an acceptable benefit can be seen (improved mentation, mucous membrane color, and arterial pres*A dobutamine infusion can be prepared in 0.9% sodium chloride or DSW. Add 220 mg of dobutamine to 500 mL of sterile isotonic fluid. Assuming intravenous fluid maintenance rate of 30 mL/lb I d, administering this infusion at 20% of maintenance rate provides 4 J.Lg/kg/min, 40% of maintenance rate provides 8 J.Lg/kg/min, 70% of maintenance rate provides 14 J.Lg/kg/min, and so forth.
Table 3. DRUGS USED IN THE TREATMENT OF CARDIOGENIC SHOCK Drug
Dose
Indication
Monitoring/Drawbacks/Precautions
Atropine
0.25-0.6 mg/kg slow IV bolus, then 5-45 !J.g/kg IV CRI 0.02-0.04 mg/kg IV
Diltiazem
0.05-0.2 mg/kg IV
Excessive effect increases heart rate or causes ventricular arrhythmias Initial brief second degree atrioventricular block possible Excessive effect causes bradycardia, hypotension
Dobutamine
2-20 !J.g/kg/min IV CRI
Dopamine
2-10 !J.g/kg/min IV CRI
Positive inotropy (increase cardiac contractility) Vagolytic-positive chronotrope (increase heart rate) Calcium-channel blocker-negative chronotrope and inotrope (decrease heart rate and contractility) Positive inotropy (increase cardiac contractility) Positive inotropy, vasoconstriction
Furosemide
2-8 mg/kg IV every 2-8 hours or same total dose as CRI
Interstitial fluid retention (pulmonary edema)
Isoproterenol
0.04-0.08 !J.g/kg/min IV CRI or 0.4 mgin250mL D5W IV CRI to effect 2.5-15.0 !J.g/kg/min IV CRI (dog) 0.5-2.0 !J.g/kg/min IV CRI (cat) 0.5-2.0-inch strip applied to skin every 8-12 hours 4 mg in 1 L of 5% dextrose given IV to effect 0.15 mg/kg IV slowly
Beta-agonists-positive chronotrope (increase heart rate)
Amrinone
Sodium nitroprusside Nitroglycerin paste Norepinephrine Phenylephrine injection Propranolol
'""'
~
ID
0.02 mg/kg
rv; repeat as needed
N = intravenous; CRI = constant rate infusion.
Arterial and venous dilation Venodilation Vasoconstriction
Excessive effect increases heart rate or causes ventricular arrhythmias Hypertension (monitor blood pressure); tachycardia; renal benefits no longer substantiated Efficacy: respiratory character, oximetry, thoracic radiographs. Possible drawbacks: electrolyte and acid-base imbalances, dehydration, hypovolemia, renal effects Excessive effect causes tachycardia Hypotension (monitor arterial blood pressure) Dubious efficacy
Vasoconstriction
Hypertension (monitor blood pressure), expensive Hypertension (monitor blood pressure)
Beta-antagonist-negative chronotrope (slows heart rate)
Excessive effect causes bradycardia, hypotension
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sure), and stop and partially reduce the infusion if negative effects such as increasing ventricular arrhythmia or worsening tachycardia are seen. Mitral Regurgitation and Cardiogenic Shock. Dogs with chronic mitral valve regurgitation maintain adequate to increased left ventricular contractility (even when disease is advanced) until exhaustion of the myocardium (myocardial failure). At this near-terminal stage, positive inotropes may be given as for decreased contractility, but severe mitral regurgitation causes part of the left ventricular stroke volume to be ejected into the left atrium with greater force during inotrope infusion. As a result, cardiogenic shock caused by mitral regurgitation and myocardial failure carries a poor to grave prognosis. Dogs rarely are presented for their first evaluation of mitral valve disease in cardiogenic shock; if they are sick enough to be in cardiogenic shock, they usually have been receiving cardiac medications chronically. For this reason, it is it essential to rule out hypovolemic shock caused by dehydration or diuretics. The latter disorder can be treated with judicious administration of intravenous fluids and medication readjustment and probably carries a slightly better prognosis than myocardial failure. Diastolic Dysfunction or Left Ventricular Hypertrophy. Because drugs that acutely correct diastolic dysfunction such as that seen in feline hypertrophic cardiomyopathy do not exist at this time, secondary conditions and contributing causes (see Table 2) are addressed when a patient with diastolic dysfunction experiences cardiogenic shock. Marked tachycardias are particularly detrimental in these diseases, where diastolic filling of the ventricle is already impaired. As a result, severe tachycardias should be addressed, first by minimizing external stimuli that cause increased sympathetic tone (place the patient in a quiet oxygen cage if appropriate) and then, if necessary, with drugs that suppress the heart rate (see section on ECG). Future directions in the management of cardiogenic shock include improved monitoring and clarification of the risks and benefits of therapy. It was recently demonstrated that pulmonary venous flow as measured noninvasively by Doppler echocardiography can more accurately reflect left atrial pressure than does pulmonary wedge pressure measurementP Confirming such a finding in clinical veterinary patients could be invaluable in more routinely assessing left atrial pressures, which, in turn, would allow optimal use of intravenous fluids and vasoactive drugs without the invasiveness and equipment needs of pulmonary wedge pressure measurement. Clinical trials assessing treatments of cardiogenic shock in veterinary medicine are entirely absent from the literature and continue to be needed. CARDIAC ARREST
Television and movies equate cardiac arrest with asystole. This misleading association conveys the impression that cardiac arrest is a
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disorder of cardiac rhythm when, in fact, it is more accurately a disorder of cardiac function. Cardiac arrest is the cessation of circulation, depriving the vital organs of oxygen. 1 The central feature of cardiac arrest is terminal circulatory dysfunction regardless of cardiac rhythm. This endstage circulatory collapse may occur with (1) asystole or severe bradycardias; (2) severe tachycardias in which the ventricles cannot fill adequately during diastole, in which case, the heartbeat is ineffective because of decreased stroke volume; or (3) relatively normal cardiac rhythms in which the electric activity of the heart is not translated into mechanical force of contraction (i.e., electromechanical dissociation) (Fig. 1). In other words, the ECG in cardiac arrest may demonstrate (1) asystole or bradycardias of sinus, atrial or junctional, or ventricular origin; (2) ventricular tachycardia or ventricular fibrillation; or (3) sinus rhythm or other supraventricular rhythms when electromechanical dissociation is present. 1, 8, 18 Rhythms in categories 2 and 3 are sometimes grouped under the heading "pulseless electric activity," because they have a common feature-visible ECG activity in the absence of effective circulation. In summary, ECG alone can provide the diagnosis of cardiac arrest when asystole is present, but it is the combination of ECG and assessment of circulation, including palpation of the pulse and measurement of the arterial blood pressure, that is usually necessary to diagnose cardiac arrest. Cardiac Arrest: Diagnosis
Because it involves cessation of effective circulation, cardiac arrest is recognized by loss of consciousness and collapse. A palpable pulse is not felt, the mucous membranes are pale or cyanotic, and respirations commonly cease (i.e., cardiopulmonary arrest). The blood pressure is too low to be measured noninvasively. ECG may demonstrate a variety of rhythms and should be used for guiding therapeutic intervention during CPR. Cardiac Arrest: Treatment
The treatment for cardiac arrest consists of instituting CPR, which has been reviewed extensively1 and is discussed elsewhere in this issue. Cardiac Arrest: Outcome
Two large retrospective clinical studies in small animal patients confirm that cardiac arrest carries a poor prognosis even with intervention.11' 22 Of 304 dogs and 95 cats experiencing cardiopulmonary arrest and receiving CPR, 11 dogs and 6 cats survived to hospital discharge (5.6% overall survival rate). The survival rate for non-anesthetic-related
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B Figure 1. Electrocardiographic tracings of rhythms consistent with cardiac arrest All lead II. A and D = 5 mm/mV; 8 and C fibrillation (25 mm/s). 8 , Ventricular tachycardia preceded by sinus beats and one VPC (25 mm/s; HR = 320/min).
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cardiac arrest is likely even lower; at least three survivors in these reports experienced cardiopulmonary arrest during general anesthesia, which implies that endotracheal intubation and immediate intravenous access were likely available. Future directions in cardiac arrest management include further understanding of events leading to a:rrest and improved treatment techniques. For example, portable cardiac monitoring has allowed an improved diagnosis of arrhythmia leading to cardiac arrest. Dogs with atrial tachyarrhythmias as a result of severe mitral valve disease were thought to experience episodes of collapse caused by paroxysmal supraventricular tachycardia, but event monitoring has revealed that the rhythm occurring at the time of collapse may be a severe bradycardia.4• 6 Such a discovery can completely alter the treatment plan. Also regarding the events leading to cardiac arrest, human beings may experience a progressive marked increase in sympathetic tone before arrest, which overpowers the effects of antiarrhythmic drugs. 17 If this were also applicable to veterinary patients, such a finding could help to explain the ineffectiveness of antiarrhythmic drugs in patients that suffer sudden arrhythmia and cardiac arrest and could provide insight into ways of monitoring and treating prearrest malignant arrhythmias. For treatment of bradycardias in a patient in cardiac arrest, an emerging noninvasive type of temporary pacemaker therapy is transthoracic pacing/ which carries the benefit of pacing without the time and fluoroscopic needs of temporary transvenous pacing. Finally, malignant and potentially lethal ventricular tachyarrhythmias may respond better to sympathetic blockade than the currently recommended Advanced Cardiac Life Support guidelines. 14 This radical change in approach, if confirmed in larger numbers of human patients and in veterinary patients, could fundamentally alter the treatment of ventricular tachyarrhythmias in cardiac arrest. References 1. American Heart Association: Guidelines 2000 for cardiopulmonary resuscitation and emergency cardiovascular care. Part 3: Adult basic life support. Circulation 102 (suppl I):Il-384, 2000 2. Binns SH, Sisson DD, Buoscio DA, et al: Doppler ultrasonographic, oscillometric sphygmomanometric, and photoplethysmographic techniques for noninvasive blood pressure measurements in anesthetized cats. J Vet Intern Med 9:405-414, 1995 3. Bodey AR, Michell AR, Bovee KC, et al: Comparison of direct and indirect (oscillometric) measurements of arterial blood pressure in conscious dogs. Res Vet Sci 61:17-21, 1996 4. Bright JM, Cali JV: Clinical usefulness of cardiac event recording in dogs and cats examined because of syncope, episodic collapse, or intermittent weakness: 60 cases (1997-1999). JAVMA 216:1110-1114, 2000 5. Califf RM, Bengston JR: Cardiogenic shock. N Engl J Med 330:1724-1730, 1994 6. Cote E, Charuvastra E, Richter K: Event-based cardiac monitoring in small animal practice. Compend Contin Educ Pract Vet 21:1025-1033, 1999 7. DeFrancesco TC, Hansen BD, Atkins CE, et al: Transthoracic temporary cardiac pacing in 42 dogs (1995-2000) [abstract]. J Vet Emerg Crit Care 10:294, 2000 8. Ettinger SJ, LeBobinnec G, Cote E: Electrocardiography. In Ettinger SJ, Feldman EC
CARDIOGENIC SHOCK AND CARDIAC ARREST
Sa. 9. 10. 11. 12. 12a. 12b. 13. 14. 15.
16. 17. 17a. 18. 19. 20. 21. 22.
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(eds): Textbook of Veterinary Internal Medicine, ed 5. Philadelphia, WB Saunders, 2000, pp 800-833 McHugh TJ, Forrester JS, Adler L, et al: Pulmonary vascular congestion in acute myocardial infarction: hemodynamic and radiologic correlations. Ann Intern Med 76:29-33, 1972 Haskins SC: Treatment of shock. In Fox PR, Sisson DD, MoYse NS (eds): Textbook of Canine and Feline Cardiology, ed 2. Philadelphia, WB Saunders, 1999, pp 272-290 Janin Y, Vetrovec G, Hess ML: Interventional therapies for cardiogenic shock. In Grenvik A, Ayres SM, Holbrook PR, et al (eds): Textbook of Critical Care, ed 4. Philadelphia, WB Saunders, 2000, pp 1037-1046 Kass PH, Haskins SC: Survival following cardiopulmonary resuscitation in dogs and cats. J Vet Emerg Crit Care 2:57-65, 1992 Kinnaird TD, Thompson CR, Munt BI: Deceleration time of pulmonary vein D wave more accurately predicts left atrial pressure than wedge pressure [abstract]. Circulation 102(suppl 11):456, 2000 Lilja GP, Clinton J, Mahoney B: MAST usage in cardiopulmonary resuscitation. Ann Emerg Med 13(9, part 2):833-835, 1984 Guyton AC, Lindsay AW: Effect of elevated left atrial pressure and decreased plasma protein concentration on the development of pulmonary edema. Circ Res 7:649-657, 1959 Meurs KM, Miller MW, Slater MR: Comparison of the indirect oscillometric and direct arterial methods for blood pressure measurements in anesthetized dogs. J Am Anim Hosp Assoc 32:471--475, 1996 Nademanee K, Taylor R, Bailey WE, et al: Treating electrical storm: Sympathetic blockade versus advanced cardiac life support-guided therapy. Circulation 102:742747, 2000 O'Connor CM, Gattis WA, Uretsky BF, et al: Continuous intravenous dobutamine is associated with an increased risk of sudden death in patients with advanced heart failure: Insights from the Flolan International Randomized Survival Trial (FIRST). Am Heart J 138:78-86, 1999 Ornato JP, Peberdy MA: The mystery of bradyasystole during cardiac arrest. Ann Emerg Med 27:576-587, 1996 Pruvot E, Thonet G, Vesin JM, et al: Heart rate dynamics at the onset of ventricular tachyarrhythmias as retrieved from implantable cardioverter-defibrillators in patients with coronary artery disease. Circulation 101:2398-2404, 2000 Rozanski EA, Dhupa N, Rush JE, et al: Differentiation of the etiology of pulmonary edema by measurement of the protein content (abstract). J Vet Emerg Crit Care 8:256, 1998 Rush JE, Wingfield WE: Recognition and frequency of dysrhythmias during cardiopulmonary arrest. JAVMA 200:1932-1937, 1992 Silver MA: Intermittent inotropes for advanced heart failure: Inquiring minds want to know. Am Heart J 138:191-192, 1999 Stepien RL, Rapoport GS: Clinical comparison of three methods to measure blood pressure in nonsedated dogs. JAVMA 215:1623-1628, 1999 Vollmar A: Prevalence and spectrum of cardiovascular abnormalities in the Irish Wolfhound: Clinical evaluation of 632 sequential cases. In Proceedings of 18th Annual Veterinary Medical Forum, Seattle, 2000, p 120 Wingfield WE, Van Pelt DR: Respiratory and cardiopulmonary arrest in dogs and cats: 265 cases (1986-1991). JAVMA 200:1993-1996, 1992
Address reprint requests to Etienne Cote, DVM Section of Cardiology Angell Memorial Animal Hospital 350 South Huntington Avenue Boston, MA 02130
0195-5616/01 $15.00
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CARDIOGENIC SHOCK AND CARDIAC ARREST Etienne Cote, DVM
CARDIOGENIC SHOCK
As cardiac disease of any type evolves, it usually passes through distinct stages. First is the asymptomatic stage, at which time there is no overt manifestation of heart disease, but medical evaluation can reveal an abnormality such as a murmur ausculted during physical examination or an arrhythmia detected on electrocardiography (ECG). Next, as progression continues, decompensation occurs. In this state, endogenous compensatory mechanisms that had sustained the asymptomatic state are overwhelmed by worsening heart disease, and perceptible abnormalities such as dyspnea or cough from pulmonary edema, syncope from an arrhythmia, or abdominal distention from cardiogenic ascites are apparent. If these abnormalities are not controlled with medication, surgery, or other therapy, further deterioration occurs and can lead to a life-threatening situation. At such an extreme, when a primary cardiac problem is responsible for inadequate systemic perfusion and the metabolic needs of the body's tissues are not met as a result of cardiac dysfunction, cardiogenic shock exists. 5' 9 Cardiogenic shock is a critical state that must be addressed urgently if the patient's life is to be saved. Causes of Cardiogenic Shock
The history of small animals that experience cardiogenic shock may or may not involve previously documented heart disease. When heart
From the Section of Cardiology, Angell Memorial Animal Hospital, Boston, Massachusetts
VETERINARY CLINICS OF NORTH AMERICA: SMALL ANIMAL PRACTICE VOLUME 31 • NUMBER 6 • NOVEMBER 2001
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disease has been documented previously, cardiogenic shock usually is the result of an acute exacerbation of the underlying problem such as rupture of a chorda tendinea or rupture of the wall of the left atrium in chronic mitral valvular disease, or severe pulmonary edema from acute ingestion of high-sodium foods or owner noncompliance with medications in cases of chronic valvular heart disease or cardiomyopathy. By contrast, when heart disease has not been diagnosed previously, a sudden onset of cardiogenic shock suggests a new, acute, or rapidly progressive cardiac problem such as acute idiopathic pericardia! effusion causing cardiac tamponade or represents a delay in seeking medical attention for a long-standing disorder. It is worth noting whether the patient in cardiogenic shock is already being treated for cardiac disease, because the treatment plan and prognosis are affected: adverse effects of medications, a more diseased heart, and fewer therapeutic options if refractory heart failure is present are more likely with advanced heart disease. In companion animals in which heart disease has been diagnosed previously, essentially any cardiac disorder, if severe enough, can lead to cardiogenic shock or cardiac arrest. The list of frequent newly diagnosed cardiac problems that are first detected when an animal is presented in cardiogenic shock is limited; cardiac tamponade from acute pericardia! effusion (idiopathic inflammatory, secondary to left atrial rupture, or malignant), chordae tendineae rupture, dilated cardiomyopathy, heartworm caval syndrome, and, occasionally, congenital malformations such as subaortic or pulmonic stenosis or end-stage patent ductus arteriosus are common in dogs, and cardiomyopathy with or without embolic disease, valvular heart disease, and, rarely, other congenital heart diseases are seen in cats. Cardiogenic Shock: Diagnosis
Cardiogenic shock is a state of severe circulatory compromise that is caused entirely by cardiac dysfunction. It is an extreme form of "forward" heart failure-the inability to generate a cardiac output sufficient to meet the body's demands. Clinical signs are referable to underperfusion of organs, particularly the brain (altered mentation consisting of disorientation, poor responsiveness, or unconsciousness), skeletal muscles (weakness, collapse), respiratory system (e.g., compensatory tachypnea due to metabolic acidosis), or heart itself (arrhythmias caused by decreased coronary circulation). An exception to this definition is a state of shock arising solely from a cardiac arrhythmia (i.e., when the heart is structurally normal). Severe hypotension caused by cardiac arrhythmia in an otherwise normal heart is classified not as cardiogenic shock but as cardiac arrest. Cardiogenic shock is confirmed when a patient has "poor cardiac output and evidence of tissue hypoxia in the presence of adequate intravascular volume." 5 In small animal medicine, such confirmation usually comes through noninvasive means, especially from the history
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and physical examination, thoracic radiography, ECG, indirect blood pressure measurement, and echocardiography. Rarely, cardiogenic shock is diagnosed in small animals as it is in human patients, in which the diagnostic criteria include (1) systemic arterial hypotension (mean <90 mm Hg for at least 1 hour and without response to intravenous fluids or a value 30 mm Hg below basal values for at least 30 minutes), (2) elevated arteriovenous oxygen difference (>5.5 mL/ dL), (3) depressed cardiac output (cardiac index <2.2 L/min/m2 body surface area) despite positive inotropic drugs, and (4) elevated pulmonary wedge pressure (>15 mm Hg). 5' 10 Physical examination of a patient in cardiogenic shock reveals an animal that on initial approach is usually either in overt distress (often showing disorientation, tachypnea, increased respiratory effort, and anxious expression) or is recumbent and poorly responsive or unresponsive. Poor perfusion is usually apparent from cool extremities and pale mucous membranes; the pulse is weak to absent as a result of poor cardiac output. Cardiac auscultation may be difficult if breath sounds are loud as a result of markedly increased respiratory effort or if pleural or pericardia! effusion is present to obscure the heart sounds. Nevertheless, a murmur or a gallop "rhythm," which is a third heart sound heard best with the bell of the stethoscope rather than the diaphragm, may be heard. This suggests increased left ventricular filling pressure and supports the suspicion of decompensated heart disease. The apex beat, or palpable heartbeat on the chest, may be diminished or absent such as in cardiac tamponade or dilated cardiomyopathy, or it may be vigorous if a large part of the left ventricle's volume is failing to reach the systemic circulation as in extreme mitral regurgitation. A vigorous apex beat in an animal with cool extremities or poor pulse quality should also prompt the consideration of noncardiac forms of shock such as hypovolemic or septic shock, requiring evaluation and treatment different from those of cardiogenic shock. Thoracic radiography is an essential part of the minimum database in a patient with cardiogenic shock. The major exception involves delaying radiography in favor of emergency treatment if obtaining the radiograph is thought to pose an immediate risk to the patient. Thoracic radiographs of a patient in cardiogenic shock answer at least two important questions: • Are there radiographic changes that support the suspicion of underlying cardiac disease? Common changes include an enlarged cardiac silhouette, atrial enlargement, and pulmonary venous and caudal vena caval engorgement. • Is there evidence of decompensation (i.e., congestive heart failure [CHF])? Such signs include pulmonary edema (left-sided CHF) and pleural effusion (left- or right-sided CHF). The clinician should be aware that the extent of cardiomegaly may be mildly attenuated by hypovolemia and possibly by tachycardia. 21 Many combinations of findings are commonly encountered. Examples
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include a large cardiac silhouette without left atrial enlargement but with small pulmonary vessels and a large caudal vena cava, which is a combination typical of pericardia! effusion; pleural effusion, pulmonary edema, and a mildly to markedly enlarged cardiac silhouette, which are frequently observed with decompensated feline heart diseases of many types; and cardiomegaly with left atrial enlargement, pulmonary venous congestion, and pulmonary edema in chronic mitral valve disease or dilated cardiomyopathy. ECG most commonly demonstrates sinus tachycardia, which is usually "appropriate"-it typically is baroreflex mediated, or aimed at increasing cardiac output in the face of critical hypotension. To deliberately suppress such a tachycardia is contraindicated, because this would likely decrease cardiac output and further exacerbate shock. Supraventricular tachycardias are actively suppressed (e.g., with intravenous propranolol or diltiazem) only when they are confirmed by a cardiologist to be self-perpetuating rhythms such as the Wolff-Parkinson-White syndrome (rare) or when they are so extreme (e.g., sustained heart rate >220-280 beats per minute in a giant- or small-breed dog, respectively, or >340 beats per minute in a cat) that adequate diastolic filling of the ventricles essentially cannot occur and the tachycardia itself contributes to the state of shock. The fine line between appropriate and excessive tachycardia is different for every patient, and suppression of an appropriate sinus tachycardia can cause cardiac arrest. Most supraventricular tachycardias in cardiogenic shock are appropriate and are best addressed with treatment of the underlying problem and concurrent issues such as hypotension, hypoxia, and acid-base or electrolyte disturbances rather than pharmacologic manipulation of the heart rate. If in doubt, the clinician can first perform a carotid sinus massage to attempt to suppress the heart rate and should note whether a more normal rate is sustained and whether pulse quality improves. Ventricular arrhythmias are also common during cardiogenic shock. Intermittent ventricular premature complexes may reflect myocardial hypoxia or similar insult and are generally not treated with antiarrhythmics. A sustained ventricular arrhythmia with hypotension and poor perfusion fulfills the criteria for cardiogenic shock or cardiac arrest, however, and is treated accordingly. As with any patient with ventricular arrhythmias, management of the patient in cardiogenic shock must involve identification and correction of any underlying problems that could precipitate the arrhythmia and make it refractory to treatment. Such problems include hypokalemia, acid-base disorders, hypoxia, disseminated intravascular coagulation, and marked anemia. Bradycardia may be the cause of cardiogenic shock or cardiac arrest, as in third-degree heart block with a slow ventricular rate, or it may be a sign of deteriorating cardiogenic shock and imminent cardiac arrest as is usually seen when a tachycardia suddenly converts to a severe bradycardia. 16 Bradycardia during cardiogenic shock should be treated with atropine (0.02-0.04 mg/kg intravenously). If this is ineffective, isoproterenol may be administered at a rate of 0.04 to 0.08 J.Lg/kg/min as a continuous rate infusion (CRI) with the dose adjusted based on
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response so as to avoid tachycardia. If the bradycardia continues to be unresponsive and the cardiogenic shock state persists, cardiac pacing may be indicated. If respirations have ceased, cardiopulmonary resuscitation (CPR) is warranted. Arterial blood pressure measurement is a cornerstone of the diagnosis and management of cardiogenic shock. The most common widely used measurement technique is Doppler ultrasonography with sphygmomanometry, which provides measurements of systolic pressure in most dogs and cats. 2• 20 In the clinical setting, the monitoring of blood pressure in a patient in cardiogenic shock must be performed continuously or as frequently as is possible without detracting from the patient's other needs (e.g., oxygen cage). Unfortunately, many criteria that could be extrapolated from human critical care medicine rely on diastolic or mean blood pressures, which are difficult or impossible to obtain by Doppler techniques. Oscillometric blood pressure evaluation measures these parameters, but results of experiments comparing this technique with direct measurement by arterial puncture have been mixed. 2• 3• 13• 20 Echocardiography greatly helps to pinpoint the lesion causing cardiogenic shock. As for any cardiac patient, the echocardiogram is often excellent at revealing the exact cardiac lesion, but fairly poor at showing the impact of that lesion on the patient. For example, echocardiography is useless for the diagnosis of pulmonary edema. In an animal in cardiagenic shock (excluding critical hypotension caused by severe arrhythmia defined previously as cardiac arrest rather than shock), echocardiography invariably reveals substantial structural heart disease. An animal suspected of having cardiogenic shock whose echocardiogram and thoracic radiographs are within normal limits probably does not have cardiogenic shock; other types of shock such as hypovolemic, distributive, or septic shock should be considered. It is common for dogs or cats with advanced cardiac disease to be treated with drugs that deplete intravascular volume, particularly diuretics. If such drugs are given in excess, or in normal doses but with decreased food or water intake, hypovolemia can occur. Hypovolemic shock induced by diuretic excess in cardiac patients is a fairly common clinical entity. When acute, this situation may be mistaken for cardiagenic shock, because such a patient may be showing signs of poor perfusion, be demonstrably hypotensive, and have physical signs of heart disease such as a heart murmur. It is important to differentiate cardiogenic shock from diuretic-induced hypovolemic shock of cardiac patients, because treatment of the former revolves around improving cardiac output, whereas treatment of the latter is based on judiciously restoring intravascular volume with intravenous fluids and close monitoring to detect recurrence of congestion (Table 1). Cardiogenic Shock: Treatment
Treatment of cardiogenic shock has one goal-to support the circulation until definitive improvement of cardiac function can be achieved.
:: UJ
~ Table 1. CLINICAL FEATURES OF CARDIOGENIC SHOCK VERSUS CHRONICALLY TREATED HEART DISEASE WITH ACUTE HYPOVOLEMIA* Cardiogenic Shock
History
Dyspnea, disorientation
Medication history
Not previously stabilized with or receiving a long-term course of cardiac medications (e.g., diuretics, digoxin, or angiotensin-converting enzyme inhibitors)
Physical examination
Thoracic radiographs
Pleural effusion or pulmonary edema
Clinical pathologic findings
Complete blood cell count/chemistry/U-A often unremarkable, respiratory alkalosis or acidosis with hypoxemia and desaturation common (pulmonary edema)
Arterial blood pressure Electrocardiogram
Low (<90 mm Hg mean)
Echocardiogram
Usually tachycardia; acute transition from tachycardia to bradycardia means cardiac arrest likely imminent
Common to Both
Anorexia, lethargy, weakness, collapse
Heart Disease and Hypovolemia
Vomiting Almost invariably receiving long-term cardiac medications (especially diuretics but also digoxin, angiotensin-converting enzyme inhibitors)
Lethargy ± collapse, tachypnea, tachycardia, poor pulse quality; murmur, gallop, arrhythmia may be present or absent Cardiomegaly
Sinus tachycardia; ventricular and supraventricular tachyarrhythmias Moderate to marked structural heart disease
Tacky/ dry mucous membranes, halitosis
Microcardia is rare because of predominant heart disease-induced cardiomegaly Azotemia and isosthenuria (diuretics ± primary renal), hemoconcentration (increased albumin and globulin, packed cell volume may be normal if hemoconcentraton and anemia of chronic disease occur jointly), metabolic acidosis Normal to low Usually tachycardia
'Some patients in a category may not show all the characteristics listed for that category. It is also worth noting that these two categories are not mutually exclusive, and that animals with deteriorating heart disease may have features of hypovolemia and cardiogenic shock.
CARDIOGENIC SHOCK AND CARDIAC ARREST
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In human medicine, long-standing improvement often is successfully achieved with definitive correction of the underlying heart disorder, including revascularization of the heart in coronary artery disease, surgical replacement of defective heart valves, resection or ablation of interventricular septal hypertrophy in hypertrophic cardiomyopathy, and cardiac transplantation. Because such long-term solutions exist, treatment of cardiogenic shock in human beings can be aimed at direct temporary relief of the inciting cause (e.g., medical dissolution of a thrombus causing myocardial infarction) and can legitimately involve sophisticated temporary techniques such as intra-aortic balloon pump implantation and left ventricular assist devices as "bridges" to a permanent solution. The technical, physical (patient size), and financial limitations of veterinary medicine are keenly apparent in the treatment of cardiogenic shock. First, there are few proven definitive corrections of underlying heart disease for which to strive in an animal with cardiogenic shock. Specific examples that do exist include relief of cardiac tamponade through pericardiocentesis, balloon pericardiotomy, or pericardiectomy; surgical removal of heartworms; and ligation or occlusion of a longstanding patent ductus arteriosus. Unfortunately, these conditions make up only a small proportion of cases of cardiogenic shock. In the absence of an intervention that can reverse the underlying cardiac problem in the long term, treatment of cardiogenic shock in animals aims to stop hemodynamic collapse in the hope that chronic medical management of heart disease can then increase longevity and quality of life. This approach has two inherent drawbacks that the clinician must recognize: the long-term benefits are not as good in the absence of definitive correction, and the prognosis probably worsens with each new occurrence of decompensation as the underlying process worsens. The primary goals of treatment are as follows: • To maintain oxygen delivery to the organs through adequate circulation • To avoid negative effects during such treatments Initial Approach To Treatment
All treatment of cardiogenic shock should involve an initial search for underlying problems that contribute to the shock state or may potentially complicate treatment (Table 2). Furthermore, because neither the natural evolution of cardiogenic shock nor the response to treatment can be predicted in a given case, ongoing monitoring during treatment is important. Monitoring techniques are essentially the same techniques as those described for the diagnosis of cardiogenic shock. In a successfully treated patient, physical examination reveals improved mentation, normalization of respiratory rate and effort, and evidence of improved peripheral perfusion such as warmer extremities and improved pulse
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Table 2. FACTORS THAT CONTRIBUTE TO OR COMPLICATE CARDIOGENIC SHOCK Factor
Hypoxia
Test
Anemia
Pulse oximetry, arterial blood gas Blood gas Serum electrolyte determination Packed cell volume
Hypoalbuminemia
Serum albumin
Pleural effusion Pericardia! effusion
Radiograph Echocardiogram
Acid-base imbalance Electrolyte imbalance
Treatment
Oxygen supplementation, improved diffusion (e.g., if edema) or improved ventilation Based on type of imbalance Appropriate intravenous crystalloid Transfusion of packed red blood cells, whole blood, or polymerized hemoglobin; control of hemorrhage if applicable Plasma transfusion, or other intravenous colloids Thoracentesis Pericardiocentesis
quality. Thoracic radiographs should demonstrate resolution of pulmonary edema if it is present, although a radiographic lag time of up to 24 hours between overt clinical improvement and radiographic improvement can occur. Arterial blood pressure should normalize, and additional hemodynamic parameters are evaluated if possible. Specifically, central venous pressure reflects the preload on the right heart and should decrease into the normal range ( <10 mm Hg) with control of right heart failure. Pulmonary capillary wedge pressure (PCWP) is obtained with a pulmonary arterial (Swan-Ganz type) catheter. The PCWP catheter is passed percutaneously into the jugular vein; under either fluoroscopic or pressure waveform guidance, it is then directed into the pulmonary artery. This procedure may be particularly challenging in smaller animals or animals with tricuspid regurgitation. Once in place, however, the catheter allows serial wedge pressure measurements to be obtained during treatment (normal range of mean PCWP: 8-14 mm Hg). Because it reflects left atrial pressure, PCWP is an invaluable tool to guide intravenous fluid administration and vasoactive drug use in patients with heart disease. A mean PCWP greater than 15 mm Hg suggests an excessive pressure load in the pulmonary venous circulation and risk of pulmonary edema; ongoing treatment to reduce PCWP is indicated. Conversely, a low or low-normal PCWP in a patient with cardiogenic shock suggests overcorrection such as occurs with excess diuretics or misdiagnosis such as occurs with noncardiogenic pulmonary edema. Reassessment of the treatment plan and intravenous fluid administration are essential when PCWP is low during management of cardiogenic shock Treatment of Specific Clinical Entities in Cardiogenic Shock
Simultaneous Hypotension and Pulmonary Edema. This situation is one of the hallmarks of cardiogenic shock, reflecting decreased cardiac
CARDIOGENIC SHOCK AND CARDIAC ARREST
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output and high left atrial pressure. Clearly, a therapeutic challenge exists, because the treatment of either abnormality can worsen the other: use of diuretics to reduce pulmonary edema further depletes intravascular volume and worsens hypotension, and intravenous crystalloid infusion or vasopressor therapy increases left heart and pulmonary venous pressures and thus increases the tendency for pulmonary edema formation. Oxygen therapy should be administered in all cases. Cardiogenic pulmonary edema should be confirmed as the sole cause for the clinical and radiographic pulmonary abnormality. Noncardiogenic pulmonary edema, or acute respiratory distress syndrome, and pulmonary hemorrhage can be mistaken radiographically for the interstitial infiltrate of cardiogenic pulmonary edema. Hemodynamic monitoring is ideal for confirming or refuting a cardiogenic cause for pulmonary edema; less optimal is evaluation of the response to diuretic therapy in the face of confirmed structural heart disease. Analysis of pulmonary secretions if expectorated or if the animal is intubated is also useful; cardiogenic edema fluid should have a total protein content lower than that of plasmaP• It is essential to address predisposing factors that could be contributing either to edema. formation or hypotension. Moderate to marked hypoalbuminemia greatly increases the tendency for pulmonary edema formation, 8 " and correction with plasma transfusion or synthetic colloids is warranted. Severe bradycardia, usually with concurrent chronic mitral valve disease, can cause pulmonary edema and arterial hypotension. Bradycardia in the face of systemic hypotension and pulmonary edema is grossly abnormal, because baroreceptor and neurohormonal mechanisms should elicit a reflex tachycardia. As a result, treatment is usually required. A positive chronotrope such as atropine (0.02-0.04 mg/kg administered intravenously) or glycopyrrolate (0.1 mg/kg administered intravenously) should be used first. If these drugs are ineffective, cardiac pacing is indicated. Increasing the heart rate to the normal range raises the cardiac output, which increases systemic arterial pressure and, barring severe structural heart disease such as marked mitral valve regurgitation, lowers left atrial pressure. Pulmonary edema and hypotension can be improved by correcting cardiac dysfunction. Unfortunately, therapeutic options remain limited and unproved. Systolic dysfunction is treated with positive inotropes such as dobutamine, although diastolic dysfunction has no effective emergent treatment. If improving cardiac function is ineffective or impossible, the more severe abnormality (pulmonary edema vs hypotension) should be treated first. Typically, this is pulmonary edema, which is treated with furosemide (2-8 mg/kg intravenously every 2-8 hours as needed). Clearly, the concurrent risk is worsening hypovolemia, with hypoperfusion of vital organs, and adjunctive measures such as the application of medical antishock trousers 12" or an equivalent external wrap may be considered (although these measures are rarely used in this setting). The use of vasodilators for managing pulmonary edema is
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relatively contraindicated in the presence of hypotension. In normotensive or mildly hypotensive patients, however, they may be used alone or in conjunction with positive inotropes. Examples of vasodilators include nitroglycerin, hydralazine, angiotensin-converting enzyme inhibitors such as enalapril, and sodium nitroprusside (see article on cardiovascular pharmacotherapy in this issue for further details). When life-threatening pulmonary edema exists in the presence of severe myocardial dysfunction, dobutamine can be used together with a potent vasodilator such as hydralazine or sodium nitroprusside. Drugs that increase arterial pressure through arterioconstriction such as phenylephrine or dopamine may be used in conjunction with measures that increase cardiac performance such as dobutamine in cases of systolic failure and severe hypotension. Because these vasopressors impose an increase in afterload on an already failing heart, using them alone (without the addition of a positive inotrope) may further exacerbate pulmonary edema. Optimal treatment is aimed at correction of the underlying cause, but unlike the case in human beings, definitive correction of hypertrophic or dilated cardiomyopathy with heart transplantation, subaortic stenosis with open-heart myotomy or myectomy, or valvular heart disease with valve repair or replacement is either impractical or simply not performed in veterinary patients. Decreased Contractility and Cardiogenic Shock. The simple solution for systolic dysfunction, or decreased contractility, of the left ventricle in the setting of cardiogenic shock is to administer drugs that increase contractility, namely, positive inotropes such as dobutamine (2-20 J..Lg/ kg/min administered intravenously as a CRI) (Table 3).* (Regrettably, these drugs also simultaneously increase myocardial oxygen demand, which predisposes to potentially malignant arrhythmias and may lead to long-term detriment.) Clinical trials of dobutamine infusion in patients with severe CHF remain divided in their findings: most show hemodynamic improvement with dobutamine (short-term benefit) but not an increase in survival (equivocal or negative long-term effect). 15• 19 The applicability of these findings to veterinary patients is unclear; the rarity of myocardial infarction in small animals may mean that patients generally have a greater amount of myocardium to respond to inotropes (beneficial), although, conversely, the absence of long-term corrections of primary heart problems may signify that the overall longevity or quality of life is not improved appreciably with inotrope infusion. In the absence of definitive guidelines, an intuitive but unproved recommendation is to begin with infusion of a low dose of an inotrope, titrate the intravenous CRI upward gradually until an acceptable benefit can be seen (improved mentation, mucous membrane color, and arterial pres*A dobutamine infusion can be prepared in 0.9% sodium chloride or DSW. Add 220 mg of dobutamine to 500 mL of sterile isotonic fluid. Assuming intravenous fluid maintenance rate of 30 mL/lb I d, administering this infusion at 20% of maintenance rate provides 4 J.Lg/kg/min, 40% of maintenance rate provides 8 J.Lg/kg/min, 70% of maintenance rate provides 14 J.Lg/kg/min, and so forth.
Table 3. DRUGS USED IN THE TREATMENT OF CARDIOGENIC SHOCK Drug
Dose
Indication
Monitoring/Drawbacks/Precautions
Atropine
0.25-0.6 mg/kg slow IV bolus, then 5-45 !J.g/kg IV CRI 0.02-0.04 mg/kg IV
Diltiazem
0.05-0.2 mg/kg IV
Excessive effect increases heart rate or causes ventricular arrhythmias Initial brief second degree atrioventricular block possible Excessive effect causes bradycardia, hypotension
Dobutamine
2-20 !J.g/kg/min IV CRI
Dopamine
2-10 !J.g/kg/min IV CRI
Positive inotropy (increase cardiac contractility) Vagolytic-positive chronotrope (increase heart rate) Calcium-channel blocker-negative chronotrope and inotrope (decrease heart rate and contractility) Positive inotropy (increase cardiac contractility) Positive inotropy, vasoconstriction
Furosemide
2-8 mg/kg IV every 2-8 hours or same total dose as CRI
Interstitial fluid retention (pulmonary edema)
Isoproterenol
0.04-0.08 !J.g/kg/min IV CRI or 0.4 mgin250mL D5W IV CRI to effect 2.5-15.0 !J.g/kg/min IV CRI (dog) 0.5-2.0 !J.g/kg/min IV CRI (cat) 0.5-2.0-inch strip applied to skin every 8-12 hours 4 mg in 1 L of 5% dextrose given IV to effect 0.15 mg/kg IV slowly
Beta-agonists-positive chronotrope (increase heart rate)
Amrinone
Sodium nitroprusside Nitroglycerin paste Norepinephrine Phenylephrine injection Propranolol
'""'
~
ID
0.02 mg/kg
rv; repeat as needed
N = intravenous; CRI = constant rate infusion.
Arterial and venous dilation Venodilation Vasoconstriction
Excessive effect increases heart rate or causes ventricular arrhythmias Hypertension (monitor blood pressure); tachycardia; renal benefits no longer substantiated Efficacy: respiratory character, oximetry, thoracic radiographs. Possible drawbacks: electrolyte and acid-base imbalances, dehydration, hypovolemia, renal effects Excessive effect causes tachycardia Hypotension (monitor arterial blood pressure) Dubious efficacy
Vasoconstriction
Hypertension (monitor blood pressure), expensive Hypertension (monitor blood pressure)
Beta-antagonist-negative chronotrope (slows heart rate)
Excessive effect causes bradycardia, hypotension
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sure), and stop and partially reduce the infusion if negative effects such as increasing ventricular arrhythmia or worsening tachycardia are seen. Mitral Regurgitation and Cardiogenic Shock. Dogs with chronic mitral valve regurgitation maintain adequate to increased left ventricular contractility (even when disease is advanced) until exhaustion of the myocardium (myocardial failure). At this near-terminal stage, positive inotropes may be given as for decreased contractility, but severe mitral regurgitation causes part of the left ventricular stroke volume to be ejected into the left atrium with greater force during inotrope infusion. As a result, cardiogenic shock caused by mitral regurgitation and myocardial failure carries a poor to grave prognosis. Dogs rarely are presented for their first evaluation of mitral valve disease in cardiogenic shock; if they are sick enough to be in cardiogenic shock, they usually have been receiving cardiac medications chronically. For this reason, it is it essential to rule out hypovolemic shock caused by dehydration or diuretics. The latter disorder can be treated with judicious administration of intravenous fluids and medication readjustment and probably carries a slightly better prognosis than myocardial failure. Diastolic Dysfunction or Left Ventricular Hypertrophy. Because drugs that acutely correct diastolic dysfunction such as that seen in feline hypertrophic cardiomyopathy do not exist at this time, secondary conditions and contributing causes (see Table 2) are addressed when a patient with diastolic dysfunction experiences cardiogenic shock. Marked tachycardias are particularly detrimental in these diseases, where diastolic filling of the ventricle is already impaired. As a result, severe tachycardias should be addressed, first by minimizing external stimuli that cause increased sympathetic tone (place the patient in a quiet oxygen cage if appropriate) and then, if necessary, with drugs that suppress the heart rate (see section on ECG). Future directions in the management of cardiogenic shock include improved monitoring and clarification of the risks and benefits of therapy. It was recently demonstrated that pulmonary venous flow as measured noninvasively by Doppler echocardiography can more accurately reflect left atrial pressure than does pulmonary wedge pressure measurementP Confirming such a finding in clinical veterinary patients could be invaluable in more routinely assessing left atrial pressures, which, in turn, would allow optimal use of intravenous fluids and vasoactive drugs without the invasiveness and equipment needs of pulmonary wedge pressure measurement. Clinical trials assessing treatments of cardiogenic shock in veterinary medicine are entirely absent from the literature and continue to be needed. CARDIAC ARREST
Television and movies equate cardiac arrest with asystole. This misleading association conveys the impression that cardiac arrest is a
CARDIOGENIC SHOCK AND CARDIAC ARREST
1141
disorder of cardiac rhythm when, in fact, it is more accurately a disorder of cardiac function. Cardiac arrest is the cessation of circulation, depriving the vital organs of oxygen. 1 The central feature of cardiac arrest is terminal circulatory dysfunction regardless of cardiac rhythm. This endstage circulatory collapse may occur with (1) asystole or severe bradycardias; (2) severe tachycardias in which the ventricles cannot fill adequately during diastole, in which case, the heartbeat is ineffective because of decreased stroke volume; or (3) relatively normal cardiac rhythms in which the electric activity of the heart is not translated into mechanical force of contraction (i.e., electromechanical dissociation) (Fig. 1). In other words, the ECG in cardiac arrest may demonstrate (1) asystole or bradycardias of sinus, atrial or junctional, or ventricular origin; (2) ventricular tachycardia or ventricular fibrillation; or (3) sinus rhythm or other supraventricular rhythms when electromechanical dissociation is present. 1, 8, 18 Rhythms in categories 2 and 3 are sometimes grouped under the heading "pulseless electric activity," because they have a common feature-visible ECG activity in the absence of effective circulation. In summary, ECG alone can provide the diagnosis of cardiac arrest when asystole is present, but it is the combination of ECG and assessment of circulation, including palpation of the pulse and measurement of the arterial blood pressure, that is usually necessary to diagnose cardiac arrest. Cardiac Arrest: Diagnosis
Because it involves cessation of effective circulation, cardiac arrest is recognized by loss of consciousness and collapse. A palpable pulse is not felt, the mucous membranes are pale or cyanotic, and respirations commonly cease (i.e., cardiopulmonary arrest). The blood pressure is too low to be measured noninvasively. ECG may demonstrate a variety of rhythms and should be used for guiding therapeutic intervention during CPR. Cardiac Arrest: Treatment
The treatment for cardiac arrest consists of instituting CPR, which has been reviewed extensively1 and is discussed elsewhere in this issue. Cardiac Arrest: Outcome
Two large retrospective clinical studies in small animal patients confirm that cardiac arrest carries a poor prognosis even with intervention.11' 22 Of 304 dogs and 95 cats experiencing cardiopulmonary arrest and receiving CPR, 11 dogs and 6 cats survived to hospital discharge (5.6% overall survival rate). The survival rate for non-anesthetic-related
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1144
COTE
cardiac arrest is likely even lower; at least three survivors in these reports experienced cardiopulmonary arrest during general anesthesia, which implies that endotracheal intubation and immediate intravenous access were likely available. Future directions in cardiac arrest management include further understanding of events leading to a:rrest and improved treatment techniques. For example, portable cardiac monitoring has allowed an improved diagnosis of arrhythmia leading to cardiac arrest. Dogs with atrial tachyarrhythmias as a result of severe mitral valve disease were thought to experience episodes of collapse caused by paroxysmal supraventricular tachycardia, but event monitoring has revealed that the rhythm occurring at the time of collapse may be a severe bradycardia.4• 6 Such a discovery can completely alter the treatment plan. Also regarding the events leading to cardiac arrest, human beings may experience a progressive marked increase in sympathetic tone before arrest, which overpowers the effects of antiarrhythmic drugs. 17 If this were also applicable to veterinary patients, such a finding could help to explain the ineffectiveness of antiarrhythmic drugs in patients that suffer sudden arrhythmia and cardiac arrest and could provide insight into ways of monitoring and treating prearrest malignant arrhythmias. For treatment of bradycardias in a patient in cardiac arrest, an emerging noninvasive type of temporary pacemaker therapy is transthoracic pacing/ which carries the benefit of pacing without the time and fluoroscopic needs of temporary transvenous pacing. Finally, malignant and potentially lethal ventricular tachyarrhythmias may respond better to sympathetic blockade than the currently recommended Advanced Cardiac Life Support guidelines. 14 This radical change in approach, if confirmed in larger numbers of human patients and in veterinary patients, could fundamentally alter the treatment of ventricular tachyarrhythmias in cardiac arrest. References 1. American Heart Association: Guidelines 2000 for cardiopulmonary resuscitation and emergency cardiovascular care. Part 3: Adult basic life support. Circulation 102 (suppl I):Il-384, 2000 2. Binns SH, Sisson DD, Buoscio DA, et al: Doppler ultrasonographic, oscillometric sphygmomanometric, and photoplethysmographic techniques for noninvasive blood pressure measurements in anesthetized cats. J Vet Intern Med 9:405-414, 1995 3. Bodey AR, Michell AR, Bovee KC, et al: Comparison of direct and indirect (oscillometric) measurements of arterial blood pressure in conscious dogs. Res Vet Sci 61:17-21, 1996 4. Bright JM, Cali JV: Clinical usefulness of cardiac event recording in dogs and cats examined because of syncope, episodic collapse, or intermittent weakness: 60 cases (1997-1999). JAVMA 216:1110-1114, 2000 5. Califf RM, Bengston JR: Cardiogenic shock. N Engl J Med 330:1724-1730, 1994 6. Cote E, Charuvastra E, Richter K: Event-based cardiac monitoring in small animal practice. Compend Contin Educ Pract Vet 21:1025-1033, 1999 7. DeFrancesco TC, Hansen BD, Atkins CE, et al: Transthoracic temporary cardiac pacing in 42 dogs (1995-2000) [abstract]. J Vet Emerg Crit Care 10:294, 2000 8. Ettinger SJ, LeBobinnec G, Cote E: Electrocardiography. In Ettinger SJ, Feldman EC
CARDIOGENIC SHOCK AND CARDIAC ARREST
Sa. 9. 10. 11. 12. 12a. 12b. 13. 14. 15.
16. 17. 17a. 18. 19. 20. 21. 22.
1145
(eds): Textbook of Veterinary Internal Medicine, ed 5. Philadelphia, WB Saunders, 2000, pp 800-833 McHugh TJ, Forrester JS, Adler L, et al: Pulmonary vascular congestion in acute myocardial infarction: hemodynamic and radiologic correlations. Ann Intern Med 76:29-33, 1972 Haskins SC: Treatment of shock. In Fox PR, Sisson DD, MoYse NS (eds): Textbook of Canine and Feline Cardiology, ed 2. Philadelphia, WB Saunders, 1999, pp 272-290 Janin Y, Vetrovec G, Hess ML: Interventional therapies for cardiogenic shock. In Grenvik A, Ayres SM, Holbrook PR, et al (eds): Textbook of Critical Care, ed 4. Philadelphia, WB Saunders, 2000, pp 1037-1046 Kass PH, Haskins SC: Survival following cardiopulmonary resuscitation in dogs and cats. J Vet Emerg Crit Care 2:57-65, 1992 Kinnaird TD, Thompson CR, Munt BI: Deceleration time of pulmonary vein D wave more accurately predicts left atrial pressure than wedge pressure [abstract]. Circulation 102(suppl 11):456, 2000 Lilja GP, Clinton J, Mahoney B: MAST usage in cardiopulmonary resuscitation. Ann Emerg Med 13(9, part 2):833-835, 1984 Guyton AC, Lindsay AW: Effect of elevated left atrial pressure and decreased plasma protein concentration on the development of pulmonary edema. Circ Res 7:649-657, 1959 Meurs KM, Miller MW, Slater MR: Comparison of the indirect oscillometric and direct arterial methods for blood pressure measurements in anesthetized dogs. J Am Anim Hosp Assoc 32:471--475, 1996 Nademanee K, Taylor R, Bailey WE, et al: Treating electrical storm: Sympathetic blockade versus advanced cardiac life support-guided therapy. Circulation 102:742747, 2000 O'Connor CM, Gattis WA, Uretsky BF, et al: Continuous intravenous dobutamine is associated with an increased risk of sudden death in patients with advanced heart failure: Insights from the Flolan International Randomized Survival Trial (FIRST). Am Heart J 138:78-86, 1999 Ornato JP, Peberdy MA: The mystery of bradyasystole during cardiac arrest. Ann Emerg Med 27:576-587, 1996 Pruvot E, Thonet G, Vesin JM, et al: Heart rate dynamics at the onset of ventricular tachyarrhythmias as retrieved from implantable cardioverter-defibrillators in patients with coronary artery disease. Circulation 101:2398-2404, 2000 Rozanski EA, Dhupa N, Rush JE, et al: Differentiation of the etiology of pulmonary edema by measurement of the protein content (abstract). J Vet Emerg Crit Care 8:256, 1998 Rush JE, Wingfield WE: Recognition and frequency of dysrhythmias during cardiopulmonary arrest. JAVMA 200:1932-1937, 1992 Silver MA: Intermittent inotropes for advanced heart failure: Inquiring minds want to know. Am Heart J 138:191-192, 1999 Stepien RL, Rapoport GS: Clinical comparison of three methods to measure blood pressure in nonsedated dogs. JAVMA 215:1623-1628, 1999 Vollmar A: Prevalence and spectrum of cardiovascular abnormalities in the Irish Wolfhound: Clinical evaluation of 632 sequential cases. In Proceedings of 18th Annual Veterinary Medical Forum, Seattle, 2000, p 120 Wingfield WE, Van Pelt DR: Respiratory and cardiopulmonary arrest in dogs and cats: 265 cases (1986-1991). JAVMA 200:1993-1996, 1992
Address reprint requests to Etienne Cote, DVM Section of Cardiology Angell Memorial Animal Hospital 350 South Huntington Avenue Boston, MA 02130