The objective of this presentation is to refresh the audience's working knowledge of what a practitioner can do to promptly identify and effectively treat cardiovascular emergency situations, such as acute left-sided congestive heart failure or cardiac tamponade. Time permitting, severe bradyarrhythmia, severe tachyarrhythmia, and systemic thromboembolism will be discussed as well. Cardiopulmonary resuscitation will not be discussed.

Decompensated left-sided congestive heart failure (L-CHF) may develop suddenly in small animals.¹ These are typically aging small-breed dogs with underlying acquired, progressive, chronic, degenerative (myxomatous) mitral valve disease, which also involves chordae tendineae and not only mitral valve leaflets. Dogs usually experience such acute decompensation following sudden rupture of one or more of the major chordae tendineae, or of several of the relatively minor ones. Cats with acquired chronic (and often aclinical up until this development) cardiomyopathy, can also go through acute decompensation, typically following an emotional, physical or hemodynamic challenge, including (but far from limited to) arterial thromboembolism. Cats (especially when young²) can experience such an event following a stressful visit to a veterinary practice or a pet groomer, or (more typically) following general anesthesia, especially one involving intravenous or subcutaneous fluid administration over several hours. Such volume supplementation can turn out to have been a true overload for these patients, even if carefully and correctly calculated. It can therefore be a major hemodynamic challenge for a cardiomyopathic cat even without the involvement of general anesthesia. A gallop rhythm can sometimes serve as a warning sign for imminent L-CHF and should therefore never be taken lightly.

Acute decompensation can develop over the course of just a few hours and may involve any combination of the following clinical signs: tongue cyanosis, sinus tachycardia, tachypnea, dyspnea, orthopnea, or open-mouthed breathing (which is more likely noticeable by the owner as an abnormality in a cat than in a dog). Typically, such decompensation, if severe enough, is extremely stressful for the patient and is likely to compromise its interest in food, play, sleep, or any activity other than mere breathing. Cyanosis in this context reflects the inability of the lung parenchyma to oxygenate pulmonary capillary blood due to severe, diffuse pulmonary edema, rather than due to a reduced cardiac output (which would result in pallor rather than in cyanosis).

When acute, severe L-CHF is suspected, thoracic radiography can establish its presence and diffusiveness but can also further compromise and actually risk the patient's life if highly anxious, and should be sometimes reconsidered or postponed, accordingly. If elected, it would make no sense to only perform one single radiograph without the benefit of viewing two orthogonal planes. In any event, a ventrodorsal position may be life-threatening in this condition, despite its known advantages when seeking lung pathology. In fact, carefully performing a dorsoventral radiograph can be much safer for the patient, not only relative to a ventrodorsal view but also relative to a lateral radiograph, and can add a great deal to our ability to assess each hemithorax in its turn without mutual superimposition.

Emergent pharmacotherapy for pets with acutely decompensated heart disease should aim for prompt improvement of blood oxygenation (e.g., by oxygen supplementation) and prompt reduction of left ventricular diastolic (filling) pressure, so as to improve ventricular compliance. This, in turn, will help reduce hydrostatic pulmonary venous pressure, congestion, and transudation. These goals can sometimes be achieved by utilizing several routes, all of which are tailored for reduction of both left ventricular preload and afterload.

Alleviation of anxiety by including opioid agents has been traditionally implemented as well, upon presentation and during oxygen supplementation, way before the administration of intravenous drugs is rendered safe enough to be attempted. While potentially contributing to better outcome, anxiolytic opioids also carry the potential risk of masking clinical signs of deterioration and should therefore be used judiciously.

If dilated cardiomyopathy is not involved, positive inotropic support is not typically needed, as the left ventricular contraction is either normal or hyperkinetic in both dogs with mitral valve disease and in cats with hypertrophic cardiomyopathy. In certain cases, however, it can help ventricular forward emptying at the expense of blood regurgitation through the mitral valve (i.e., at the expense of pulmonary venous pressure), given that afterload has been decreased beforehand, or at least in parallel to this process. One should keep in mind, however, that in cats with a loud systolic murmur due to hypertrophic obstructive cardiomyopathy (HOCM), positive inotropic support may actually be contraindicated and should not be attempted until HOCM has been ruled out.³

When feasible, constant rate infusion or repeated bolus administration of intravenous diuresis can not only promptly reduce cardiac preload and therefore reduce ventricular filling pressure,⁴ but can also directly dilate pulmonary veins, thereby contributing even further to the reduction of intravenous hydrostatic pressure and relief of dyspnea, even before diuresis takes place⁵. This should help reduce transudation of plasma into the lung parenchyma. The respiratory rate should be closely monitored and frequently documented, and diuretic dose and/or frequency should be decreased as soon as this rate just begins to decrease, even if not yet normalized. This practice should be helpful in reducing the risk of developing secondary dehydration, azotemia, and hypokalemia.

Oral pimobendan (if practical and if not contraindicated) can contribute to and accelerate the resolution of L-CHF, especially when firstly "loaded" using a high dose, as its bioavailability is relatively high and its serum concentration builds up relatively fast.⁶

Nitrates such as nitroglycerin have been a popular component of the therapeutic regimen when managing acute L-CHF patients, not because of their potency (which is actually not high enough to make a tangible difference when administered as monotherapy) but rather due to their noninvasive (and hence, non-stressful) administration. The only available nitrate that is highly potent is sodium nitroprusside (SNP), which is also "balanced" (i.e., it dilates arterioles as well, not mostly veins). This agent is capable of reducing both preload and afterload and also carries the advantage of having a very short half-life, which makes it safe as well. Unlike many other intravenous drugs, however, its dose should be gradually increased as long as there is an ongoing, documented clinical improvement, rather than being increased only "to effect." This is counterintuitive to most clinicians, who only seldom increase its dose once they notice an improvement in their patient's condition. This is likely the reason why many become disappointed with its performance, and choose to abandon its use before acquiring enough experience with it to use it again in other patients. When SNP administration results in systemic hypotension, the dose should be decreased and only re-increased once intravenous dobutamine (or high-dose dopamine) is added through a different vein, with incremental dosing as needed to maintain blood pressure stability, while taking care to avoid high enough dobutamine or dopamine doses to provoke arrhythmia.

Some highly tachypneic and dyspneic patients develop severe respiratory muscle fatigue and require ventilator therapy under general anesthesia to provide them with the temporary respiratory muscle relief they need until recovery.^7,8

Cardiac tamponade, whether idiopathic or a complication of mitral valve regurgitation leading to left atrial wall rupture or of neoplasia, is a potentially life-threatening condition. It can dangerously compromise cardiac output, not by hampering the force of heart contraction but rather by limiting venous return and diastolic filling volume. While it may develop gradually (often with resultant ascites and without necessarily triggering an acute state of shock) or acutely (typically triggering acute shock), it can also develop slowly but exacerbate acutely. The faster the accumulation of fluid inside the pericardial sac, the less compliant it is, hence, the lower volume required to build a high enough intrapericardial pressure to compromise cardiac output. Because of the exponentially decreasing pericardial sac compliance, the later the stage in the process (even if chronic), the faster the pressure buildup in that sac. Accordingly, the later the stage, the faster the development of hemodynamic compromise. An acutely accumulating low volume can trigger an extremely high pressure and severely threaten life, while a chronically accumulating effusate can reach a large volume before it poses any true threat. Therefore, it is not the amount of volume we identify, but rather the clinical and/or imaging evidence of pressure present within the pericardial sac, that should dictate our sense of urgency. Imaging modalities such as cardiac ultrasound would attest to such a high pressure by demonstrating a collapsing right atrium, and in more severe cases, a collapsing right ventricle as well (ideally imaged from the left apical four-chamber view). However, clinical examination findings such as those compatible with a shock state that present along with (the clinically counterintuitive) peripheral venous congestion, and more importantly, a paradoxical arterial pulse, can sometimes be readily identifiable way before imaging is made possible, and should therefore alert us and increase our index of suspicion of cardiac tamponade.

If no mitral regurgitation is suspected, aggressive intravenous fluid administration should be considered even prior to pericardiocentesis, and especially if such centesis fails or cannot be performed. Diuretic therapy, on the other hand, should be avoided as it cannot readily reach the isolated pericardial space and can actually exacerbate the compromise of venous return and cardiac output.

References

1.  Serres F, Chetboul V, Tissier R, Sampedrano CC, Gouni V, Nicolle AP, Pouchelon JL. Chordae tendineae rupture in dogs with degenerative mitral valve disease: prevalence, survival, and prognostic factors (114 cases, 2001–2006). J Vet Intern Med. 2007;21(2):258–264.

2.  Schmiedt CW, Holzman G, Schwarz T, McAnulty JF. Survival, complications, and analysis of risk factors after renal transplantation in cats. Vet Surg. 2008;37(7):683–695.

3.  Gordon SG, Saunders AB, Roland RM, Winter RL, Drourr L, Achen SE, Hariu CD, Fries RC, Boggess MM, Miller MW. Effect of oral administration of pimobendan in cats with heart failure. J Am Vet Med Assoc. 2012;241(1):89–94.

4.  Nelson GI, Silke B, Forsyth DR, Verma SP, Hussain M, Taylor SH. Hemodynamic comparison of primary venous or arteriolar dilatation and the subsequent effect of furosemide in left ventricular failure after acute myocardial infarction. Am J Cardiol. 1983;52(8):1036–1040.

5.  Opie LH, Kaplan NM, Poole-Wilson PA. Diuretics. In: Opie LH, Gersh BJ, eds. Drugs for the Heart. 5th ed. Philadelphia, PA: W.B. Saunders Co.; 2001: 84–106.

6.  Suzuki S, Fukushima R, Ishikawa T, Hamabe L, Aytemiz D, Huai-Che H, Nakao S, Machida N, Tanaka R. The effect of pimobendan on left atrial pressure in dogs with mitral valve regurgitation. J Vet Intern Med. 2011;25(6):1328–1333.

7.  Corredor C, Jaggar SI. Ventilator management in the cardiac intensive care unit. Cardiol Clin. 2013;31(4):619–636.

8.  DeFrancesco TC. Management of cardiac emergencies in small animals. Vet Clin North Am Small Anim Pract. 2013;43(4):817–842.