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Small Animal Emergency and Critical Care Medicine: A Colour Handbook ( Veterinary Color Handbook Series): Medicine & Health Science.
Table of contents

Delaney Editor Call Number: Hand Editor ; Craig D. Thatcher Editor ; Rebecca L. Novotny Editor Call Number: Small Animal--Nutrition. Island Bats by Theodore H. Fleming Editor ; Paul A. Racey Editor Call Number: Warren Call Number: Ws Guillermo Couto Call Number: Q. Lorenz Editor ; T.

Morrison Call Number: Q. Henry Call Number: Argyle Editor ; Malcolm J. Brearley Editor ; Michelle M. Turek Editor Call Number: Dobson Call Number: Withrow; Rodney Page; David M. Vail Call Number: Q. Sumner-Smith Call Number: Grimm Editor ; William J. Tranquilli Editor ; Leigh A. Lamont Editor Call Number: Forensic Toxicology by W. Lowry Call Number: Maddison Editor ; Stephen W. Page Editor ; David B. Church Editor Call Number: Poppenga Editor ; Sharon M. Gwaltney-Brant Editor Call Number: Symposium on clinical toxicology for the small animal practitioner by Oehme, Frederick W.

Call Number: Veterinary Medicine [non-circulating] Peck; Denis J. Marcellin-Little Call Number: Robertson Call Number: F. Graham Call Number: Instructions for Veterinary Clients by David L. Erlewein; Eugene L. Introduction to Veterinary Genetics by Frank W. Nicholas Call Number: Keene; Francis W. Smith; Larry P.

Tilley; Bernie Hansen Call Number: Small Animal Cardiology by O. Lynne Nelson Call Number: Pichler Editor Call Number: Burk; Daniel A. Feeney; Norman Ackerman Call Number: Manual of acupuncture for small animals. ISBN: Gilchrist, David. Greyhound acupuncture. Mareeba, Australia: Pro-Prom Pty. The Holistic Guide for a Healthy Dog. Howell Books, University of Minnesota, Messonnier, Shawn P. Natural Therapy for an Arthritic Dog.

Keats Publishing, King Editor Call Number: Simpson Editor ; Gary C. England Editor ; Mike J. Harvey Editor Call Number: Petersen-Jones Editor ; Sheila M. Niemiec Call Number: Mosby's Series. Need help? Veterinary Medicine Library. Email Me. Contact: S. Lincoln Ave. Subjects: Veterinary Medicine. Cowell; Amy C. Valenciano Call Number: Interpretation of laboratory results for small animal clinicians by Bush, B. Sodikoff Call Number: Percy; Stephen W. Swing; Rena Marr; Felipe M.

Berard; Andrew G. Cawthon Call Number: Suckow Editor ; Karla A. Stevens Editor ; Ronald P. DuPont; Linda J. Cardioversion is painful in dogs and should only be attempted in dogs that are unconscious or lightly anesthetized. Cardiac emergencies Cardiopulmonary resuscitation Congestive heart failure in the dog Congestive heart failure in the cat Cardiac arrhythmias Pericardial effusion Arterial thromboembolism Syncope Differential diagnoses.

Animals often have severe underlying disease prior to arrest, rather than sudden ventricular fibrillation as may affect people. The ultimate goal of CPR is to restore spontaneous, effective cardiac and respiratory efforts. Respiratory arrest develops when ventilatory failure leads to a loss of consciousness that, unless corrected, rapidly leads to combined CPA.

The arrhythmia may be the result of primary cardiac disease e. Thromboembolic disorders, such as PTE or thromboembolic disease to the coronary arteries, are other possible causes of sudden, otherwise unexplained CPA. A pre-existing cardiovascular, respiratory, or CNS disorder is typically present in dogs and cats with spontaneous CPA. Following CPR in any individual case, it can be informative to review the factors present before arrest e. It is useful to review these factors, and learn from the arrest, in order to better recognize and treat contributing CPA risk factors in future cases and be better able to avoid CPA in future cases.

Isolated respiratory arrest is present when failed ventilatory effort leads to agonal breathing and then loss of consciousness, although cardiac function is present and arterial pulses are palpable. Defibrillate as soon as ventricular fibrillation is identified at any time during CPR. Pulses Reconsider whether major intervention needed, i.

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Obstructions to the airway are usually immediately apparent during endotracheal intubation, and in cases of fixed upper airway obstruction i. The endotracheal tube should have the cuff filled in order to ensure adequate manual ventilation, and the endotracheal tube should eventually be secured in place to prevent dislodgement as the animal is turned for defibrillation or other maneuvers. Suctioning of the airway may be required for animals with massive edema, and animals can be briefly tipped into a head-down vertical position, with brief chest compressions, in order to help drain edema fluid from the airway.

Immediate adjustments to the rate or effort of manual or mechanical ventilation can be made following assessment of the amount of pressure required to fill the lungs and the degree of rise and fall of the thorax. Inadequate filling of the endotracheal cuff is a common cause for inadequate rise of the chest wall with low pressure, and pneumothorax should be a differential diagnosis if increases in ventilatory pressure develop during CPR.

Respiratory alkalosis from excessive ventilation should be avoided.

Manual or mechanical ventilation should be continued until long after the onset of spontaneous respiratory efforts. Following CPA, most animals will not have effective respiratory drive or ventilatory effort at the time that they first start to breathe on their own or start to chew on the endotracheal tube. It is advised that a very low dose of diazepam or a narcotic be given to permit ongoing intubation, and that manual or mechanical ventilation be continued for at least 20 min following the onset of spontaneous efforts at ventilation. The authors do not recommend use of acupuncture points and do not recommend cessation of ventilation in order to determine whether the animal is able to breathe using its own effort at any time during the CPR effort.

All animals that eventually recover will breathe on their own, and. Following intubation, initiation of breathing, and confirmation of cardiac arrest, efforts at cardiac compression should be initiated. CPR is ideally performed with the animal in right lateral recumbency to facilitate venous return to the heart. In some small-breed dogs more effective cardiac compressions can be achieved using one hand on either side of the thorax, instead of two hands on top of the thorax with the table as the base to press against. In cats the heart can often be stabilized and compressed using a single hand with the thumb on one side of the thorax and three fingers on the other side of the chest.

For medium- to large-breed dogs both hands are usually placed higher on the chest wall and the chest and heart are compressed between the table and the hands. The more dorsal hand location in large-breed dogs is based on the recognition that effective compressions may occur from either the cardiac pump mechanism direct cardiac compression or the thoracic pump mechanism increase in intrathoracic pressure forces blood out of the chest cavity and valves prevent retrograde flow.

It is suspected that direct cardiac compression can be achieved in cats and small-breed dogs; however the thoracic pump mechanism may be more important for large-breed dogs. Some authors recommend dorsal recumbency with compression of the sternum during CPR for medium- to large-breed dogs; however, the authors have not found this technique to be more effective and have not adopted it in their institution. The duty cycle, or duration of compression to relaxation, should be approximately with equal time devoted to each phase.

A large number of adjunctive CPR procedures have been proposed and include techniques such as interposed abdominal compression, activecompressiondecompression CPR, simultaneous. It is still acceptable, and it is the authors routine practice, to employ standard CPR and to make no serious attempt to coordinate the chest compressions and the ventilations. Successful cardiac compression is documented by palpation of femoral or lingual arterial pulses If pulses are not identified then CPR efforts should be evaluated and adjusted. The temptation to stop chest compression to check on the cardiac rhythm should be resisted as each stoppage of CPR leads to a rapid 35 s drop in blood pressure and it requires s of CPR before blood pressure returns to the prior CPR-effected level.

Hand position and compression effort can be adjusted prior to the identification of a cardiac rhythm; however the authors recommend ECG evaluation prior to administration of drugs or initiation of open-chest CPR in most cases. Ventricular fibrillation is only effectively treated with electrical DC defibrillation.

Defibrillation should be attempted as soon as the rhythm is identified, as any delay in defibrillation rapidly reduces the chance of a successful conversion. Epinephrine should not be routinely administered prior to defibrillation. Energy required for internal defibrillation during open-chest CPR is much lower with a recommended dose of J. An initial defibrillation effort should be followed by evaluation of the cardiac rhythm, and an immediate repeat shock at the same energy should be attempted if ventricular fibrillation persists.

Asystole is recognized by a total lack of cardiac activity. Asystole is treated with continued cardiac compression and administration of epinephrine. In this dog, one person is performing ventilation with an Ambu bag, another is checking for femoral arterial pulses, one is performing chest compressions, and another is drawing blood to check for correctable abnormalities in serum electrolytes, pH, or blood glucose. An ECG is being recorded, the dog has just received a dose of epinephrine intravenously, and intravenous fluids are being administered to restore recent blood loss.

EMD is recognized as an electrocardiographically identifiable rhythm that is not accompanied by palpable arterial pulses EMD can be the result of inadequate venous return to the heart due to hypovolemia, cardiac tamponade, or tension pneumothorax, or it may result from severe acidosis, myocardial hypoxia, or severe myocardial dysfunction, hypoxia, or ischemia. EMD due to myocardial disease is rarely reversible, however efforts to identify and treat hypovolemia, pleural or pericardial space disease, metabolic or respiratory acidosis, and severe electrolyte imbalance can often be rewarding.

Sodium bicarbonate may be useful in animals with EMD or asystole and known pre-existing acidosis or hyperkalemia, and calcium administration can be used in animals with known or documented hypocalcemia or hyperkalemia. Sinus bradycardia can be treated with atropine, and if this is ineffective then epinephrine can be administered.

Ventricular tachycardia that develops during the course of CPR should be assessed for heart rate and the presence of a pulsegenerating rhythm. Epinephrine Epinephrine has long been a recommended therapy for dogs and cats with CPA. The positive inotropic and chronotropic effects of epinephrine stimulate cardiac contractile function via -receptors, and epinephrine stimulates -receptors to create vasoconstriction and increases in blood. It may be that the -mediated effects of epinephrine are more important than the mediated effects in some cases. The increase in blood from vaso-constriction leads to improved coronary and cerebral blood flow.

The enhanced vasoconstriction seen with higher doses of epinephrine 0. High-dose epinephrine 0. It also increases the risk for epinephrine-induced ventricular fibrillation. For these reasons, most authors currently recommend use of standard-dose epinephrine initially 0. If this dose is ineffective then epinephrine administration can be repeated every 23 min with dose escalation until the desired response is achieved.

Vasopressin New research supports the use of vasopressin antidiuretic hormone during CPR to improve vascular tone and blood pressure. The proposed dose in dogs is 0. Further research is required in order to determine whether epinephrine, vasopressin, or a combination of the two drugs is most useful for CPR. Fluids Routine administration of large volumes of crystalloid fluids during CPR may not be required for successful outcome. In fact, animals known to have pre-existing cardiac failure, respiratory failure with pulmonary edema or infiltration, or CNS edema formation may be adversely affected by administration of large volumes of crystalloid or colloid fluids during CPR.

Prior to administration of fluids during CPR, some effort should. Fluid administration is clearly appropriate for animals with known hypovolemia. Crystalloid fluids or colloids can be useful in normovolemic animals that develop loss of effective circulating volume due to fluid pooling in venous structures shortly after CPR. The volume of fluid returning to the heart is easily assessed during open-chest CPR based on palpation of cardiac filling during the diastolic phase of manual compression, however this can be very difficult to evaluate during closed-chest CPR.

Open-chest cardiac compression Open-chest CPR can result in significantly greater increases in cardiac output when compared with closed-chest CPR. However, there is little evidence that open-chest CPR will improve outcome. In addition, open-chest CPR leads to a huge resource and personnel utilization and creates an entirely new set of complications not seen with closed-chest CPR. There are certain clinical settings where early open-chest CPR is indicated or preferred and these include CPA associated with tension pneumothorax, large-volume pleural effusion, flail chest, diaphragmatic hernia, and cardiac tamponade.

If the decision has been made that the owner wishes to proceed to open-chest CPR if closed-chest CPR is unsuccessful then the clinician is advised to make this decision early, in the first 5 min after closed-chest CPR is initiated. A step-by-step description of open-chest CPR is beyond the scope of this chapter, however the following advice is offered based on observation of multiple efforts by a variety of individuals: The incision made is often too far forward and this can make it difficult to grasp the heart the incision must be at either the fifth or sixth intercostal space.

Entry to the thorax in a somewhat uncontrolled fashion often leads to lung lobe laceration, therefore care is advised for this step. It can be difficult to grasp and incise the pericardium, an essential step for good open-chest CPR, and laceration of the myocardium, coronary artery, or atrium may occur when this incision is made in a poorly controlled fashion. The heart should be compressed in an apical to basilar fashion in order to maximize the effectiveness of compressions.

The individual performing cardiac massage should make a conscious effort to assess cardiac filling during diastole to assess the need for more fluids. In addition, the degree of cardiac tone and vigor of contraction can be assessed which allows for feedback to others participating in CPR relative to inotropic state and the need for inotropic therapy.

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In most cases, the author finds that a component of active diastolic filling with increased cardiac tone will precede the onset of effective systolic contractile function. Post-resuscitation care A critical factor in successful CPR is the effort of those involved in post-resuscitation care. A repeated episode of CPA is common, and to avoid a repeat arrest it is usually essential to identify at least one major contributing factor to the arrest and eliminate this factor.

Possible examples of risk factors that could be corrected include some of the following: Pleural space disease is corrected by centesis. Anemia is treated with transfusion. Respiratory failure is managed with mechanical ventilation. Narcotics are reversed and then either discontinued or used in lower doses. Infusions of positive inotropes, like dopamine or dobutamine, are indicated for animals with hypotension or myocardial depression.

In severe CHF, either sodium nitroprusside or intubation and intermittent positive pressure ventilation may be successful. Consider thoracocentesis if suspect pleural effusion; consider pericardiocentesis if muffled heart sounds. Repeat furosemide. Left-sided CHF develops in dogs with elevated left heart filling pressures and leads to pulmonary edema with or without small-volume pleural effusion. Right-sided CHF occurs in dogs with elevated right heart filling pressures and is manifest as ascites with or without pleural effusion.

Most dogs with large-volume pleural effusion have biventricular heart failure with elevated right and left heart filling pressures. Acquired chronic valvular disease, or endocardiosis, primarily affects the mitral valve, although up to one third of affected dogs have both mitral and tricuspid regurgitation. Pericardial effusion is also a cause of CHF, usually in large-breed dogs. Dogs with congenital heart disease may also develop CHF, as can dogs with bacterial endocarditis and a variety of uncommon cardiac disorders. Large- and giant-breed dogs are predisposed to dilated cardiomyopathy.

The condition has also been recognized in Cocker Spaniels. Small and medium-size breeds of dogs are predisposed to chronic valvular disease. CHF is more usual in middle-aged to older dogs, but can develop as a result of congenital disease; dilated cardiomyopathy can be seen within the first few years of life. In general, there is a slight predisposition for the development of CHF in male dogs.

This elevated pressure is transmitted back to the venous system and the elevated capillary pressures lead to fluid exudation into the interstitium and edema formation. Left-sided CHF, most commonly observed as pulmonary edema in dogs 13 , often develops after the left ventricular or left atrial filling pressures rise above mmHg. In some dogs, chronic left heart failure leads to elevations in pulmonary arterial pressures and biventricular heart failure develops. Biventricular heart failure is identified as combined pulmonary edema, pleural effusion, and ascites.

Note the expectorated pulmonary edema. Additional historical complaints for dogs with CHF may include tachypnea or dyspnea, syncope, lethargy or exercise intolerance, abdominal distention, anorexia, and weight loss. While some dogs have slow development of clinical signs, it is common for clinical signs to appear more acutely. Physical examination findings Dyspnea, cough, and ascites may be noted. Femoral arterial pulses are often weak and the jugular vein is typically distended above the bottom third of the neck in dogs with right-sided or biventricular heart failure.

Pulmonary crackles are often present on auscultation in dogs with pulmonary edema, and dogs with pleural effusion may have dull lung sounds ventrally. CHF in the dog is often associated with an S3 gallop A murmur of mitral or tricuspid valve regurgitation is the most frequent murmur noted on auscultation, and the murmur is often loud in. The first and second heart sounds are the normal heart sounds S1 and S2 , with S1 occurring shortly after the onset of the QRS complex and S2 occurring near the end of the T wave.

The S3 gallop, present in early diastole, is the result of rapid cessation of passive diastolic ventricular filling and is often heard in dogs with dilated cardiomyopathy or in dogs with chronic valvular disease at the onset of CHF. The gallop is best noted using the bell of the stethoscope. The systolic murmur of mitral regurgitation is depicted by the red band between S1 and S2. Arrhythmias with pulse deficits, mucous membrane pallor, or delayed capillary refill time may also be noted.

Some dogs with CHF have a recent unplanned weight loss. In the authors practice, bronchitis is an infrequent diagnosis in mature to older large-breed dogs, and dilated cardiomyopathy with mild CHF should be a key differential in this setting. It is worth noting that echocardiography alone is generally not sufficient to diagnose CHF, and auscultation of the lungs for pulmonary crackles is also an unreliable method for diagnosing CHF. Radiography The key findings on thoracic radiographs 15 that can lead to a diagnosis of CHF are: Cardiomegaly. Pulmonary venous distention. Caudal vena cava distention.

Perihilar pulmonary infiltration. In dogs, the first radiographic evidence of leftsided CHF is an interstitial pattern, which can be difficult to distinguish from the aging pulmonary interstitial changes that are seen in many dogs. Resolution of this interstitial pattern following furosemide administration can be a method for distinguishing the two clinical entities.

As CHF progresses, a bronchial pattern may be noted in many medium- to large-breed dogs; this is followed by overt alveolar flooding, which results in radiographic air bronchograms. Pleural effusion or ascites is usually evident in dogs with biventricular or right-sided CHF. Additional testing Additional diagnostic testing that is recommended for dogs suspected of having CHF includes an ECG and an echocardiogram. Baseline laboratory testing, including a CBC and serum biochemistry profile with electrolytes, is also recommended. Electrocardiogram Findings from the ECG are not specific for CHF but can include a left atrial or left ventricular enlargement pattern, conduction disturbances, such as bundle branch block, and cardiac arrhythmias are common Serum biochemistry Modest elevations of BUN or creatinine may result from prerenal azotemia due to inadequate cardiac output or prior diuretic administration, elevated liver enzymes may be noted due to chronic passive hepatic congestion, and mild hypoproteinemia is common in dogs with ascites.

There is moderate generalized cardiomegaly with left atrial enlargement. The perihilar interstitial and alveolar pulmonary infiltrate is characteristic of cardiogenic pulmonary edema in dogs.

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The ventricular arrhythmia resolved and sinus rhythm was present following treatment with sotalol. Echocardiography The key echocardiographic finding to confirm a diagnosis of cardiogenic pulmonary edema in dogs is dilation of the left atrium. In dogs suspected to have right-sided CHF, dilation of the right atrium should be easily visualized, except in dogs with pericardial effusion. A variety of additional findings may be present and are usually specific to the type of heart disease that has led to CHF 17, Thoracocentesis should be performed in dogs with pleural effusion that is of sufficient volume that it likely contributes to dyspnea.


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Dogs with large-volume ascites may benefit from abdominocentesis, especially if the ascitic fluid is limiting respiratory effort or lung volume. Cage rest is indicated, and supplemental oxygen can be administered through a number of methods. There is recent enthusiasm for administration of furosemide via a CRI. A CRI of furosemide can be dosed at 0. Sodium nitroprusside The most effective drug for dogs with severe pulmonary edema refractory to standard treatment is sodium nitroprusside.

This drug is used for 13 days while other therapies for management of CHF are being initiated. The mitral valve is thickened and prolapses a beyond the mitral valve annulus. There is enlargement of the left atrium b and ventricle c. Nitroglycerine Nitroglycerine glyceryl trinitrate can be administered transcutaneously to the inner surface of the ear pinna, the inguinal region, or even smeared directly onto the oral mucous membranes. Additional treatment When these initial measures for emergency management of CHF are ineffective then sodium nitroprusside, dobutamine, or mechanical ventilation can be used.

The turbulent flow of blood back into the left atrium is indicative of mitral regurgitation. Side effects can include sinus tachycardia, supraventricular or ventricular tachyarrhythmias, and GI side effects. Mechanical ventilation In selected cases, mechanical ventilation can be a very successful adjunct to the other therapies. Mechanical ventilation with use of positive endexpiratory pressure should be considered in any dog judged to be at imminent risk for CPA.

It allows for control of the airway and avoidance of respiratory failure leading to respiratory arrest while other therapies are being performed. Positive end-expiratory pressure is useful in helping to clear pulmonary edema. Mechanical ventilation requires adequate equipment in addition to ventilator skills and a significant commitment of time and resources. Long-term management For chronic management of CHF, exercise limitation, dietary sodium restriction, diuretic therapy, and ACE inhibitors usually form the backbone of therapy.

Cough, often due to left atrial enlargement, may be a troublesome longterm management concern 19, There is marked cardiomegaly and the considerably enlarged left atrium arrowheads causes dorsal displacement of the trachea a and carina b , and compression of the mainstem bronchus c. Many dogs respond well to initiation of medications and dietary recommendations, while others fail to respond or encounter repeated side effects or bouts of CHF.


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To some degree, the dedication of the owner and the owners financial means can play a big role in the outcome for dogs with CHF. While a 2-year survival is possible for some dogs with chronic valvular disease, a 6-month to 1-year survival might be more typical once CHF has developed. In dogs with dilated cardiomyopathy the survival is often shorter than that of dogs with mitral regurgitation due to chronic valvular disease. In one study, the median survival was only 2 months, and several studies have identified a particularly short survival time for Doberman Pinschers.

Still, with dedicated owners who are willing to make several adjustments to therapy, survival beyond 6 months is possible for many dogs with dilated cardiomyopathy. For dogs with CHF due to uncorrectable congenital heart disease the long-term survival is often only a few months with medical therapy alone. Stressful maneuvers, such as phlebotomy and catheter placement, should be delayed for several hours.

The radiographic location of pulmonary edema can be variable in cats with CHF. Many cats with CHF can survive well beyond 1 year following initiation of successful management. Ultrasonography in the emergency room can be useful to identify the presence of pleural effusion or left atrial enlargement. Leftsided CHF develops in cats with elevated left heart filling pressures and leads to pulmonary edema with or without a small to moderate volume of pleural effusion and, rarely, pericardial effusion.

Right-sided CHF occurs in cats with elevated right heart filling pressures. Most cats with large-volume pleural effusion have biventricular heart failure with elevated right and left heart filling pressures. Endocarditis is an uncommon cause of CHF. Some cats with heartworm disease will develop right-sided CHF. Middle-aged, male cats are predisposed to hypertrophic cardiomyopathy, and surveys of cats with hypertrophic cardiomyopathy.

Recent corticosteroid administration, especially long-acting formulations of prednisone prednisolone , can precipitate CHF in otherwise compensated individuals. Trauma, intravenous fluids, and recent surgery or anesthesia with ketamine can also predispose to the development of CHF. There is marked hypertrophy of the interventricular septum b and left ventricular free wall d , and the left ventricular internal lumen c is decreased in size. CHF develops following a rise in ventricular diastolic filling pressures, which is transmitted back to the pulmonary veins or systemic veins.

This leads to elevated capillary pressures and edema formation. Left-sided CHF is most commonly seen as pulmonary edema in cats, although a small to moderate volume of pleural effusion develops in some cats. Biventricular heart failure leads to pleural effusion with or without pulmonary edema and smallvolume ascites. Large-volume ascites of cardiogenic origin in cats is uncommon.

Dyspnea is recognized by some owners; however, lethargy, reduced food intake, and limited interaction with family members e. Overt dyspnea in some cats is not apparent until the travel to or visit at the veterinarian. Additional possible historical complaints for cats with CHF are syncope, intermittent open-mouth breathing, reduced exercise tolerance before open-mouth breathing, abdominal distention, and, occasionally, weight loss in cats with pleural effusion or ascites.

Cough is an uncommon presenting complaint for cats with CHF.

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Feline asthma, heartworm, or lungworm should be considered as more likely diagnoses in cats with cough. Physical examination findings Dyspnea is often the most prominent initial finding on initial evaluation of cats with CHF. Harsh lung sounds with pulmonary crackles are typically present in cats with pulmonary edema. Cats with pleural effusion of cardiogenic origin often have muffled lung sounds on the ventral thorax, hepatomegaly, and jugular vein distention. Femoral arterial pulses are often weak and mucous membranes can be pale or cyanotic.

Rectal temperature is often low. Auscultation of the heart can be an important contributor to the diagnosis of CHF as a soft murmur, a gallop, or arrhythmia is often present Cardiac murmurs in most feline heart. Feline asthma. Lymphosarcoma and other primary or metastatic neoplasia. Heartworm disease. Pulmonary contusions. Diaphragmatic hernia. The first and second heart sounds are normal S1 and S2 , with S1 occurring shortly after the onset of the QRS complex and S2 occurring near the end of the T wave.

The S4 gallop is present in late diastole, after the P wave, and is the result of atrial contraction of blood into a stiff and hypertrophied ventricle. The gallop is often heard best using the bell of the stethoscope. Many cats have a soft, systolic cardiac murmur near the left or right sternal border and the murmur is depicted by the blue band between S1 and S2. There is an interstitial to consolidating alveolar infiltrate in the perihilar lung fields and the pulmonary vasculature is engorged, findings that are typical of cardiogenic pulmonary edema. Cardiomegaly is evident and the liver is also enlarged.

Radiography Thoracic radiographic findings that are typically present in cats with CHF include cardiomegaly and pulmonary infiltrates. Cardiomegaly is most readily identified on the dorsoventral radiographic view with reduced cardiothoracic index due to atrial enlargement. In cats with left-sided CHF both pulmonary arteries and veins become distended. Perihilar pulmonary infiltration, commonly noted in dogs with cardiogenic pulmonary edema, is a less consistent finding for cats Pulmonary edema can develop in the perihilar region, or in the ventral lung fields, or edema may be noted to have a patchy distribution in one or more lung lobes.

A bronchial pattern is uncommon in cats with CHF and should instead lead to consideration of asthma, lungworm, or heartworm. Pleural effusion is identified by pleural fissure lines, lung lobe retraction from the chest wall, partial collapse of the cranial lung lobes, and loss of the cardiac silhouette The caudal vena cava may become distended, however the presence of pleural effusion can obscure observation of the cava and hepatomegaly may be a more reliable radiographic indicator of CHF.

Cardiomegaly is present; this is difficult to confirm, however, due to silhouetting of the heart in the pleural effusion. On the lateral thoracic radiograph the caudal lung lobes are partially collapsed and retracted away from the spine arrowheads. The liver is enlarged. On the dorsoventral view the cranial lungs lobes are nearly completely collapsed due to pleural effusion and the lungs are retracted away from the chest wall arrowheads.

There are several rib fractures that can be appreciated on the dorsoventral view in the right caudal thoracic wall just to the left of the arrowheads, and these fractures likely resulted from increased respiratory effort associated with dyspnea. The combination of interstitial to alveolar pulmonary infiltrates and small-volume pleural effusion is strongly suggestive of a diagnosis of CHF.

Additional testing Additional diagnostic testing recommended in cats with presumptive CHF includes blood pressure, an ECG, and an echocardiogram. Cats with a deep S wave in lead II should have multiple leads obtained to determine whether a right axis shift or left anterior fascicular block pattern is present. Mild elevation of BUN or creatinine may be identified but this is more common after initiation of medical treatment.

Ultrasonography Ultrasonography can be very useful in the emergency setting to confirm the presence of either pleural effusion or significant atrial enlargement. Moderate to marked left atrial enlargement is virtually always present in cats with cardiogenic pulmonary edema 25, The concentric hypertrophy present in cats with hypertrophic cardiomyopathy, the most common cause of heart failure in cats, is also relatively easy to identify via echocardiography.

Echocardiography is the best tool to determine the specific cause of cardiac disease and to rule in or rule out cardiac disease as the cause of the clinical signs. The aorta a and semilunar valves are evident in the center, with the enlarged right atrium b and right ventricle c above the aorta, and the markedly enlarged left atrium d and left auricular appendage e below the aorta. The image is from a similar orientation as in the necropsy specimen in There is marked enlargement of the left atrium and left auricular appendage e. Oxygen therapy, appropriate doses of furosemide, nitrates, and thoracocentesis for cats with moderate to large volumes of pleural effusion are the key treatment approaches in most cases Limited stress is a crucial aspect of emergency care for dyspneic cats suspected to have CHF.

Transcutaneous nitroglycerine glyceryl trinitrate can be used and is administered as 36 mm 0.

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Blood should not be drawn, an intravenous catheter should not be placed, and if radiographs have not yet been obtained then it is advised that 13 hours of initial treatment and oxygen cage stabilization be allowed before radiography is attempted. Cats are very susceptible to stressinduced deterioration of dyspnea, especially when they have first arrived in a new and unfamiliar environment. Once dyspnea is improved then it is safer to place an intravenous catheter and perform additional testing.

Empiric thoracocentesis is not recommended for cats with pulmonary crackles; however, thoracocentesis prior to radiography may be appropriate for a cat with dull lung sounds ventrally, a distended jugular vein, and hepatomegaly, that is breathing with shallow respirations at an expanded lung volume. Additionally, cats that have had pleural effusion in the past are likely to develop it again. Additional treatment In cats that fail to respond to initial management then additional treatment approaches can include a CRI of furosemide, intravenous enalaprilat or sodium nitroprusside.

Although some cats with CHF have physical evidence of dehydration based on abnormal skin tent , elevated PCV or total solids, or azotemia, fluid therapy is not warranted in a cat with CHF. There is a dramatic reduction in the volume of pleural effusion and the lung lobes are more fully expanded. The liver has decreased in size. Enalapril Enalapril is usually considered to be more effective as a chronic medication for CHF and is not indicated in an emergency setting.

However, the authors have seen some cats with severe pulmonary edema respond favorably to 0. Sodium nitroprusside This is useful for cats that fail to respond to initial intravenous doses of furosemide. A CRI of nitroprusside is administered at a dose of 0. To limit stress, blood pressure measurement is commonly not performed as long as the cat appears to be resting comfortably. Dobutamine Dobutamine can also be used in cats but, due to frequently observed toxicities of vomiting and seizures, the drug is usually reserved for echocardiographically confirmed systolic dysfunction.

Mechanical ventilation As described for dogs, mechanical ventilation can be used in cats with pulmonary edema when CPA seems imminent. Some cats with severe, life-threatening pulmonary edema can respond very well to treatment and may live for 3 years or longer. In other cases CHF is the proximate cause of death at the time of the first hospitalization. Other cats respond poorly or experience side effects of medications and short-term survival or euthanasia is the result.

As with dogs, in some cases the dedication and financial means of the owner can play a big role in the outcome for cats with CHF. Cats with pleural effusion and those with more severe left atrial enlargement appear to have a reduced survival. All normal cardiac rhythms originate from the sinus node. In addition to sinus rhythm, sinus arrhythmia and second degree AV block can be normal rhythms in the dog. Sinus bradycardia is often observed in healthy large-breed dogs at rest, and sinus tachycardia is seen with excitement or exercise.

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