Collapsing dogs: managing common causes of collapse or syncope (Proceedings)


Collapse and shock are a clinical manifestation of many different severe diseases, and requires emergency triage and care. Other dogs may present with a history of episodes of collapse and may be clinically stable on presentation. These two categories of patients are treated very differently, but they have some similar differential diagnoses.

Collapse and shock are a clinical manifestation of many different severe diseases, and requires emergency triage and care. Other dogs may present with a history of episodes of collapse and may be clinically stable on presentation. These two categories of patients are treated very differently, but they have some similar differential diagnoses.

A clinical algorhythm for the collapsed hypotensive dog includes: cardiogenic shock, hypovolemic shock, or distributive shock. Cardiogenic shock is uncommon, and may be seen with acute severe heart disease or end-stage heart disease of many etiologies. Systolic myocardial failure and low output heart failure is seen with severe dilated cardiomyopathy. The most important diastolic disease leading to cardiogenic shock is pericardial effusion and cardiac tamponade. Other diastolic heart diseases that cause cardiogenic shock in cats includes hypertrophic cardiomyopathy and restrictive cardiomyopathy. Heart diseases that cause severe volume overload such as acute severe mitral regurgitation and a major chordae tendinae rupture, or acute infective endocarditis of the mitral or aortic valves may cause cardiogenic shock. Severe sustained tachyarrhythmias or bradyarrhythmias decrease cardiac output and can cause cardiogenic shock. Transient tachyarrhythmias or bradyarrhythmias may cause transient decreased cerebral perfusion and syncope (see below) rather than sustained collapse and shock. Hypovolemia may be secondary to hemorrhage or many diseases that cause severe dehydration and a volume underloaded state. Distributive shock occurs when there is inappropriate vasodilation, and main causes include sepsis and anaphylaxis.

The initial triage of the collapsed patient includes measurement of vital parameters, blood pressure, pulse oximeter, electrocardiogram, and STAT minimum database (CBC, chemistry including electrolytes). If possible urine should be collected for urinalysis. A FAST scan of the abdomen and the thorax is useful to quickly evaluate for free abdominal fluid, pleural effusion, or pericardial effusion. Abdominocentesis should be done to evaluate for hemorrhagic effusion, and the fluid saved to submit for fluid analysis if indicated. In animals with low clinical suspicion of cardiogenic shock and heart failure, placement of a large bore intravenous catheter and shock bolus of intravenous crystalloids (60-90 ml/kg) should be given while additional diagnostics are done. In addition to evaluating for pericardial effusion, a triage echocardiogram is also used to evaluate for severe myocardial failure in dogs with dilated cardiomyopathy and cardiogenic shock. In dyspnic animals, the left atrial size should be assessed either subjectively or quantified by measurement of the ratio of the left atrial diameter to the aortic diameter in the right parasternal short- axis basilar view. Normal LA:Ao is <1.5, and significant left atrial dilation is >1.8. Dogs with severe mitral regurgitation and cardiogenic pulmonary edema typically have severe left atrial dilation (LA:Ao ≥ 2) except in the rare instance of acute major chordae tendinae rupture.

Cardiac arrhythmias

Severe arrhythmias are typically readily apparent on an ECG and require immediate life-saving treatment.

Severe tachyarrhythmias

Sustained ventricular tachycardia requires acute antiarrhythmic therapy and hospitalization. Lidocaine is the drug of choice (2-4 mg/kg IV, repeated to 6 mg/kg total cumulative dose followed by CRI 40-80 mcg/kg/min). Intravenous procainamide, esmolol, or amiodarone are other choices for refractory ventricular arrhythmias. Potassium levels should be assessed, as hypokalemia lessens the efficacy of lidocaine and should be corrected. Once the arrhythmia is stabilized, an echocardiogram should be done to assess whether there is severe myocardial failure, pericardial effusion and tamponade, or a cardiac mass. Identification of severe myocardial failure aids choice of the most appropriate chronic antiarrhythmic drug, since dogs with severe dilated cardiomyopathy cannot tolerate beta blockade. In these patients, choices are limited to mexilitene (5-7 mg/kg PO BID), flecainide (5 mg/kg PO TID), or amiodarone (10 mg/kg PO BID x 7 days then 5 mg/kg PO q24 hr), or very slow up-titration of sotalol. In dogs with normal systolic function, my first choice for antiarrhythmic drug is sotalol, and other choices include atenolol or the previously mentioned antiarrhythmic drugs. Sotalol or the combination of atenolol and mexilitene effectively decreases the severity of arrhythmia and reduces syncopal episodes in Boxer dogs with arrhythmogenic right ventricular cardiomyopathy.(5) Follow-up ECG and ideally holter monitoring is important after starting antiarrhythmic medication for continued chronic management. Often combination antiarrhythmic therapy is needed, such as sotalol and mexilitene, or amiodarone and low dose atenolol or mexilitene.

Terminal arrhythmias include asystole, where there is lack of any electrical cardiac activity, and ventricular fibrillation. Both should be treated aggressively with immediate cardiac defibrillation (5-10 joules/kg extrathoracic), as well as emergency drugs including atropine and epinephrine. Asystole has very little chance of cardioversion, given the lack of electrical activity. If there is refractory ventricular fibrillation, bretylium may be a last resort.

Supraventricular tachycardia (SVT) is caused by an ectopic atrial focus or a re-entrant pathway involving the AV node or an accessory pathway. SVT may be initiated by a P wave that appears different from the sinus nodal P wave, and may be negative or buried in the preceeding T wave. PR interval may be different than the sinus derived PR interval. Often SVT has a rapid rate of 200-300 bpm, and typically has an abrupt onset and termination. SVT in cats is often 300-400 bpm. SVT often causes syncope, and requires emergency treatment with intravenous antiarrhythmics including IV diltiazem (0.125-0.25 mg/kg slow IV over 1-2 minutes, repeating dose if ineffective) or esmolol (0.25-0.5 mg/kg IV over 1-2 minutes). Cardioversion may be another option for refractory SVT. Ideally, an echocardiogram is done to assess myocardial function, since beta blockers should not be given if there is severe myocardial failure. Choices, in order of preference, for chronic therapy include diltiazem (1-4 mg/kg PO TID, often high doses are needed), atenolol (1-2 mg/kg PO BID) and sotalol (1-3 mg/kg PO BID). Chronic tachycardia >180 bpm for longer than a couple of weeks may lead to pacing induced myocardial failure, which is indistinguishable from idiopathic dilated cardiomyopathy (DCM) on echocardiography. Tachycardiomyopathy, however, is rapidly reversible once rate control has been established. Atrial fibrillation appears as an irregular, often very fast supraventricular rhythm with absence of P waves. In most dogs except giant breed dogs, it is secondary to severe underlying heart disease, and often dogs with marked tachycardia have concurrent congestive heart failure. Antiarrhythmic therapy is aimed at decreasing the AV nodal conduction by prolonging AV nodal conduction time and refractory period, which decreases the number of wavelets that depolarize the ventricles. Typically oral therapy is used, although intravenous diltiazem may be given in the extremely tachycardic and unstable emergency patient. Chronic oral therapy is used to maintain the heart rate ≤140 bpm, and choices include: diltiazem (0.5- 3 mg/kg PO TID, starting at low dose), atenolol (0.5-2 mg/kg PO BID), or sotalol (1-3 mg/kg PO BID). Once again, it is important to assess myocardial function by echocardiography prior to giving a beta blocker, as dogs with severe dilated cardiomyopathy cannot withstand beta blockade. If an echocardiogram is unavailable, the safest choice for antiarrhythmic therapy is diltiazem +/- digoxin. Digoxin increases vagal tone and may aid in slowing the ventricular response rate, but is not usually adequate to maintain adequate rate control in severely tachycardic cases.

Severe bradyarrhythmias

High grade second degree atrioventricular block and third degree atrioventricular block are the most common bradyarrhythmias that cause collapse in small animals. High grade 2DAVB consists of frequent non-conducted P waves and there are never 2 consecutively conducted P waves (can describe the ratio of P's to QRS, such as 2:1, 3:1) which causes significant bradycardia. Third degree AV block (3DAVB) is evidenced by lack of any association of P waves with QRS complexes, and is caused by severe AV nodal disease. Nodal escape beats have a supraventricular morphology and typically a rate of 40-60 bpm in dogs, and 80-100 in cats. Purkinge escape beats are wide and bizarre, ventricular beats occurring at a slower rate of 20-40 bpm in dogs, and 60-80 bpm in cats. Patients with high grade 2DAVB and 3DAVB often present for lethargy, collapse, or syncope. Lidocaine or other ventricular antiarrhythmic therapy (beta blockers, mexilitene, sotalol) is contraindicated for treatment of 3DAVB, even if there are ventricular premature beats, as it will likely eliminate the life-saving purkinge escape beats. Dogs with high grade 2DAVB have equal risk to dogs with 3DAVB for sudden death, and have a 30% risk of dieing suddenly within 6 months of diagnosis regardless of whether clinical signs are present. Atropine 0.04 mg/kg IV should be given to animals with these bradyarrhythmias, although it is unlikely to cause an increase in the ventricular rate since the atrioventricular node is almost always severely diseased in these cases. Dogs with high grade 2DAVB and 3DAVB should be treated with a permanent pacemaker.(1)

Sick sinus syndrome (SSS) typically causes syncope rather than sustained collapse, and it is the most common arrhythmia in Schnauzers and Cocker Spaniels. SSS is composed of several arrhythmias, with sinus arrest (pause > 2 x RR interval) the signature of the disease. Other abnormalities include: sinus bradycardia, sinus arrhythmia, first and second degree atrioventricular block (2DAVB). Supraventricular tachycardia (SVT) may preceed sinus arrest (i.e. tachy-brady syndrome). Syncope usually occurs when there is a pause of sinus arrest of ≥ 6 seconds. An atropine challenge test is necessary to help differentiate sinus bradycardia or sinus arrhythmia due to high vagal tone from SSS. High dose atropine (0.04 mg/kg SC) is given and the ECG repeated 30 minutes later. Dogs with high vagal tone have regular sinus tachycardia, with HR ≥ 140, and no pauses of sinus arrest or AV block. Dogs with SSS often have pauses of sinus arrest or suboptimal increase in rate (<130 bpm). If there is a significant atropine response and the resting rate is slow (<65), terbutaline, a nonselective beta agonist, can be given. If there is no clinical improvement, other anticolinergic agents such as propantheline could be given. Asymptomatic dogs with SSS have a significant risk of sudden death during general anesthesia, and require either a temporary pacemaker or isoproterenol constant rate infusion (CRI). A permanent pacemaker is the treatment of choice for symptomatic dogs with SSS.

Pericardial effusion

Cardiac tamponade secondary to severe pericardial effusion is an important cause of collapse in dogs. The most common presenting complaint of dogs with pericardial effusion is collapse, weakness, syncope, or lethargy. Dogs often (50% of patients) present with abdominal distension and ascites secondary to cardiac tamponade. Heart sounds are muffled, and lung sounds may also be muffled if there is pleural effusion. Femoral pulses are weak, and sometimes pulsus paradoxis may be palpated when the pulse is stronger during exhalation and weaker during inhalation. If there is cardiac tamponade, the animal may have signs of cardiogenic shock including pale mucous membranes, cold extremities, hypotension, tachycardia, and collapse. These cases require immediate triage for emergency diagnostics and treatment. An intravenous catheter should be placed and shock doses of fluids given. Immediate pericardiocentesis is necessary in dogs with low output heart failure and collapse. The animal is placed in left lateral recumbency, and triage basic level echocardiography is used to define the most optimal site for pericardiocentesis (usually at the right 5th intercostal space at the costochondral junction), where there is greatest amount of pericardial fluid the furthest away from the heart and great vessels. In animals that are stable and do not have signs of cardiac tamponade, it is advisable to postpone pericardiocentesis until a detailed echocardiogram is done, as long as it is within a relatively short period of time. An ECG should be recording the rhythm during the pericardiocentesis. Pericardial effusion is almost always hemorrhagic (except for infectious etiologies) and a small sample should be placed in an FDP tube (preferable over a RTT) since it will immediately clot if it is an intracardiac sample. Fluid should also be saved to submit for fluid analysis and cytology.

A detailed echocardiogram is necessary to evaluate for cardiac masses, and localization of the mass to specific anatomic regions such as the heart base or right atrium is very critical to provide prognostic value. In a study of 107 dogs diagnosed with pericardial effusion, echocardiography was sensitive (80%) and specific (100%) for detection of a cardiac mass, and was equally sensitive (84%) and specific (100%) for distinguishing right atrial masses from all other etiologies, or distinguishing heart base masses from all other etiologies (sensitivity 74% and specificity 98%).

Etiology of pericardial effusion

Neoplasia was the most common cause of pericardial effusion (71% of dogs). Hemangiosarcoma was the most common etiology of pericardial effusion (34%), followed by idiopathic pericarditis (20%), mesothelioma (14%), chemodectoma (8%), thyroid adenocarcinoma (6%), infective pericarditis (5%), lymphoma (3%), sarcoma (2%), and 1 case of each of the following: carcinomatosis, ruptured left atrium secondary to severe mitral regurgitation, sterile foreign body, and granuloma. 33% of cases of mesothelioma had discrete cardiac masses, most often of the heart base (4/5) and rarely of the right atrium (1/5). A majority of right atrial masses were hemangiosarcoma (35/40 dogs, 88%), followed by 1 case (2.5%) of each: neuroendocrine tumor, thyroid adenocarcinoma, mesothelioma, lymphoma, and sarcoma. Heart base masses were most often neuroendocrine tumors (40%), followed by thyroid adenocarcinoma (25%), mesothelioma (20%), and hemangiosarcoma (15%). 1 dog had concurrent right atrial hemangiosarcoma and a neuroendocrine heart base mass. The pericardial masses were caused by one case each of lymphoma and a granuloma. The right ventricular mass was an undifferentiated sarcoma. 3 of 5 cases of infective pericarditis were caused by fox tail foreign bodies with secondary bacterial infections.

Survival analysis

Based on echocardiographic classification, dogs with no cardiac mass lived longer (MST 10.1 months) than dogs with echocardiographic evidence of a cardiac mass (MST 0.5 months, P= 0.0001) Dogs with a heart base mass diagnosed by echocardiography lived longer (MST 5.2 months) compared to dogs with a right atrial mass diagnosed by echocardiography (MST 0.03 months, P= 0.0002) All deaths recorded were caused by the specific etiology of the pericardial effusion and not due to other systemic disease. Regarding specific etiologies of pericardial effusion, dogs with non-neoplastic etiologies lived longer (MST 24.83 months) than dogs with neoplastic etiologies (MST 0.63 months, P < 0.0001). Dogs with hemangiosarcoma had shorter survival (MST 0.07 months) than all other neoplastic etiologies combined (MST 5.17 months, P= 0.0001). Survival time of dogs with mesothelioma was not different from dogs with heart base masses including chemodectoma, ectopic thyroid, or non-specific etiology (MST 6.5 months vs. MST 5.17 months respectively, P= 0.51).

Cardiogenic shock

Dogs with severe dilated cardiomyopathy, or less commonly acute severe mitral regurgitation due to a myxomatous valve degeneration and a ruptured chordae tendiate or infective endocarditis of the mitral or aortic valves, may present with low output heart failure with marked hypotension and concurrent congestive heart failure. Dobutamine constant rate infusion (3-10 mcg/kg/min) is given, as well as pimobendan (0.25-0.3 mg/kg PO BID). Acute hemodynamic effects of pimobendan including increased cardiac output, systemic vasodilation, and pulmonary vasodilation, may be seen as soon as 30 minutes – one hour after oral administration. In dogs with severe mitral regurgitation, sodium nitroprusside (1-10 mcg/kg/min, starting low and up-titrating based on blood pressure measurement) is also helpful to acutely decrease afterload and lessen the severity of the mitral regurgitation and elevation of pulmonary capillary wedge pressure. Aggressive diuresis with high dose furosemide (4-6 mg/kg IV q 1-4 hours or CRI of 1 mg/kg/min) is necessary in dogs with fulminant heart failure.

The syncopal dog

Many of the same etiologies described above that cause collapse in the dog may also cause a transient decrease in cerebral perfusion and syncope. Classic characteristics of syncope include a transient decrease in vasomotor tone resulting in recumbency, possible loss of consciousness, and abrupt and quick recovery within seconds to a couple of minutes. Unlike seizures, dogs do not typically hypersalivate or display nystagmus, do not have a pre-ictal and post-ictal phase, but may urinate, deficate, and have tonic muscles. Sometimes syncope can lead to a seizure if there is a lack of blood flow to the brain for a prolonged period of time of several minutes. The algorhythm for cardiogenic syncope includes abnormalities causing pressure overload to the heart (subaortic stenosis, pulmonic stenosis, pulmonary hypertension), severe tachyarrhythmias (ventricular tachycardia, atrial fibrillation, supraventricular tachycardia), severe bradyarrhythmias (sick sinus syndrome, second degree atrioventricular block, third degree atrioventricular block, atrial standstill), or low output heart failure (dilated cardiomyopathy). An atypical seizure is another differential for syncope, and sometimes the distinction between seizure versus syncope can be challenging. Evaluation for significant cardiac abnormalities is the first priority, as anesthesia is not necessary and life-threatening abnormalities may be readily identified. An ECG, blood pressure, radiographs, and a high level echocardiogram are all essential cardiac modalities to diagnose the cause of episodes of collapse. A holter monitor or event monitor are useful to evaluate intermittent arrhythmias, and are done when there is no defined etiology of the collapsing episodes based on echocardiogram and baseline ECG.

Pulmonary hypertension is a very important cause of syncope, and is challenging to diagnose. A high level echocardiogram may identify pathognomic abnormalities such as concentric and eccentric right ventricular hypertrophy, septal flattening, pulmonary artery dilation. In animals with normal pulmonary artery blood flow velocity (i.e. no pulmonic stenosis), measurement of an increased velocity of tricuspid regurgitation (> 3 m/s) confirms pulmonary hypertension, and severity is typically defined based on the pressure gradient. Mild pulmonary hypertension (TR pressure gradient <50 mmHg) does not typically cause syncope or require specific therapy. Moderate and severe pulmonary hypertension (50-75 mmHg and >75 mmHg respectively) often cause syncope, and are typically treated with sildenafil (1-2 mg/kg PO TID). Further systemic evaluation is needed to assess for a procoagulable state, underlying pulmonary disease, or severe left heart disease, which provide additional therapeutic targets. Prognosis for moderate or severe pulmonary hypertension is very poor, and survival is often weeks to several months.

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