Objectives of the Presentation
Review the clinical skills and tests used to diagnose cardiac disease and congestive heart failure (CHF).
Summarize current knowledge, opinion, and controversies about when and how to treat CHF.
Encourage therapeutic decisions based upon clinical findings, not the disease you assign to a patient.
Encourage a conservative approach to therapy that involves owner participation.
Encourage healthy dose of skepticism—don’t believe everything you hear or read.
Key Clinical Diagnostic Points
Auscultation is a sensitive screening test for cardiac disease; it is a relatively insensitive and nonspecific test for diagnosing congestive heart failure.
Pulmonary crackles in dogs are most commonly caused by pulmonary fibrosis, not pulmonary edema.
Coughing, although sometimes caused by CHF, is not commonly caused by CHF.
Elevated heart rate and/or respiratory rate accompanied by dyspnea, abdominal distension, or muffled heart sounds should markedly increase suspicion of congestive heart failure.
Assessing respiratory rate, in cooperation with owners, is a powerful monitoring tool.
Elevated jugular venous and central venous pressure or hepatojugular reflux suggests right heart failure.
Radiography is an important tool for detecting CHF and monitoring efficacy of therapy.
Visualize ascites, pleural effusion, and pulmonary interstitial and alveolar infiltrates.
Detect enlargement of intrathoracic pulmonary and/or systemic veins, and enlarged liver/spleen.
Ultrasonography can noninvasively define the anatomy and severity of cardiac disease as well as detect pleural and peritoneal effusions and hepatic venous engorgement.
In the presence of ascites or pleural effusion, right heart enlargement and enlarged hepatic veins support a diagnosis of congestive heart failure.
In the presence of pulmonary edema or pleural effusion (cats>dogs), left heart, especially left atrial, enlargement supports a diagnosis of congestive heart failure.
In the absence of dysrhythmia, electrocardiography adds little to the diagnosis of cardiac disease or CHF.
In cats, but not in dogs:
CHF is a relatively uncommon cause of ascites.
Hypothermia is common in patients with CHF whereas hyperthermia is very uncommon.
Chylothorax is a common manifestation of CHF that responds to therapy for CHF.
Key Etiologic and Pathophysiologic Points
Cardiac lesions (anatomical or functional) do not immediately or always lead to CHF.
Many patients with significant heart disease will never develop congestive heart failure.
HEART FAILURE is a clinical syndrome and should not be considered a final diagnosis.
Heart failure comes in two forms: congestive (CHF) and low output.
CHF is present when there is increased pulmonary venous capillary (left heart failure) or central venous pressure (right heart failure) as a result of significant cardiac pathology.
RIGHT SIDED CHF is characterized by elevated central venous pressure and manifests as:
Ascites—common in dogs, uncommon in cats
Peripheral edema—not a prominent finding in small animals
LEFT SIDED CHF is characterized by elevated pulmonary venous pressure and manifests as pulmonary edema (and, although a controversial concept, pleural effusion in cats).
BIVENTRICULAR CHF is characterized by elevated systemic and pulmonary venous pressures and can manifest as any of the above signs or pleural effusion.
SYSTOLIC DYSFUNCTION is an impaired ability to eject blood from the ventricle(s).
DIASTOLIC DYSFUNCTION is an impaired ability of the ventricle(s) to fill.
Many clinicians erroneously associate CHF with myocardial failure or systolic dysfunction when, in fact, many patients with CHF have no evidence of myocardial failure or systolic dysfunction.
CHF may result from anatomical or functional systolic, or diastolic dysfunctions.
Congestive heart failure is common in diseases that lead to left heart volume overload (patent ductus arteriosus (PDA), aortic regurgitation, mitral regurgitation, and less commonly, ventricular septal defect).
CHF is uncommon in left heart pressure overloads (aortic stenosis, systemic hypertension).
CHF is uncommon with mild to moderate tricuspid regurgitation in the absence of an obstruction to right ventricular ejection such as pulmonic stenosis (PS) or pulmonary hypertension (PH).
CHF is not uncommon in cases of severe right heart volume overload (atrial septal defect, tricuspid regurgitation), especially when combined with an obstruction to right ventricular ejection. (PS or PH)
Right-sided CHF is not uncommon in patients with acute pulmonary hypertension, advanced heartworm disease, or diseases of the pericardium.
Patients with primary myocardial failure (dilated cardiomyopathy) will commonly live years with few to no clinical signs. CHF or sudden death is a common end-stage event in these patients.
CHF, often due to decompensation of underlying cardiac disease may be observed in high output states (e.g., hyperthyroidism, anemia, pregnancy).
Key Therapeutic Points
The goals of treatment are to:
Whenever possible eliminate or reverse the underlying anatomical (e.g., ligate a PDA, treat dirofilariasis, etc) or functional defect (supplement with taurine in cases of taurine deficiency myocardial failure in cats and some dogs, treat hemodynamically significant arrhythmias, etc.).
Reduce capillary filling pressures adequately to eliminate or reduce edema accumulation while keeping the patient healthy and functional (a balancing act).
The tools of treatment are:
Physical manipulations: whenever possible, remove all fluid from the pleural and abdominal space for diagnostic purposes and to relief the patient of discomfort or distress.
Drugs that help achieve the above stated goals.
Diet: supplement with taurine and/or carnitine in appropriate situations (myocardial failure in the face of suspected or proven deficiency). Avoid high sodium intake.
Surgery: short of prevention, the most potent therapy for congenital and valvular conditions. Our ongoing dependence upon drugs reflects inadequate skill and resources.
Classes of drugs commonly used to treat CHF:
Diuretics: not very sexy but, by far, our most powerful “weapon.”
Goal: to reduce intravascular volume and lower venous capillary pressures.
Commonly used agents: furosemide, spironolactone, hydrochlorothiazide.
Efficacy: the only class we can say, without hesitation, saves lives.
Pure Vasodilators: quite useful for acutely “unloading” the heart and promoting forward flow.
Goal: to promote forward flow, reduce regurgitation, and lower venous pressures.
Commonly used agents: hydralazine, amlodipine, nitroprusside (acute IV).
Efficacy: nitroprusside can “buy” us time acutely—but they can’t go home on it; amlodipine may fulfill the promise of hydralazine without the GI side effects.
Angiotensin Converting Enzyme Inhibitors: great adjunctive therapy but overrated and oversold.
Goal: to inhibit retention of salt and water via the renin-angiotensin-aldosterone system.
Commonly used agents: enalapril, lisinopril, benazepril.
Efficacy: preventive or monotherapy unproven. Diuretic + ACEI = standard CHF therapy.
Positive inotropes: years of disappointment but pimobendan may redeem our hopes.
Goal: to enhance cardiac pump function and efficiency.
Commonly used agents: digoxin, dobutamine, dopamine.
Efficacy: digoxin, the mainstay of oral therapy for centuries is a pretty weak inotropes in dogs and cats; dobutamine and dopamine may be beneficial IV for acute short-term “support”; milrinone never made it to mainstream; pimobendan may finally be “it.”
Strategies for patients with cardiac disease but not in congestive heart failure:
There is no evidence that early (prior to the onset of CHF) medical treatment of asymptomatic cardiac patients with chronic valvular disease alters patient quality or quantity of life.
Whether there is benefit to early (prior to the onset of CHF) medical treatment of dogs with dilated cardiomyopathy with ACE inhibitors or cats with hypertrophic cardiomyopathy with calcium entry blockers or beta-blockers remains controversial.
Strategies for patients presenting in congestive heart failure:
Strategies for palliative therapy (i.e., diuretics, vasodilators, positive inotropes, paracentesis, etc.) are often the same regardless of the underlying dysfunction or disease.
Diuretics, primarily furosemide, continue to be the mainstay of therapy with modulators of vasomotor tone and neuroendocrine mediators being of supplemental value.
Cardiac tamponade in patients with pericardial effusion is an exception where palliative drug therapies for CHF may be detrimental. Pericardiocentesis should be pursued first.
In all patients, strategies addressing the underlying anatomical or functional defect should be aggressively pursued if there is adequate evidence to suggest a positive influence on quality and quantity of life.
Background and Detail
Pathophysiology of congestive heart failure:
(Note: to keep the following in perspective, remember that the “business end” of the cardiovascular system is the capillaries and their interaction with the body’s tissues. The heart and all the other vessels we focus upon exist as pumps and tubes to service this function.)
A process and a continuum: Cardiac lesions (anatomical or functional) do not immediately or always lead to CHF.
Early response to “the insult”:
Reduced cardiac output (CO) and/or arterial pressure (AP) triggers compensatory mechanisms.
Early, short-lived and energetically expensive, sympathetic responses compensate to normalize CO and arterial pressure (AP) via increased heart rate, force of contraction and vasoconstriction.
Longer term (hours to days), more long-lived, less energetically expensive, compensatory mechanisms include activation of the renin-angiotensin-aldosterone system (RAAS), arginine vasopressin (ADH), low level chronic stimulation of the sympathetic nervous system, and local vasoconstrictor systems.
RAAS and ADH stimulated fluid accumulation and venoconstriction of the large capacitance venous vessels, if unchecked, would result in elevated cardiac venous and capillary pressures with the net result being an imbalance in forces driving net fluid movement outward across the capillary, resulting in formation of edema (CHF). Atrial natriuretic peptide (ANP) counters these effects in part.
Concurrently, altered cardiac preload and afterload stimulates cardiac remodeling (concentric or eccentric hypertrophy) to normalize cardiac wall stress (systolic and diastolic, respectively).
The asymptomatic, well-compensated patient:
The desired result of these compensatory mechanisms is a return toward normal CO and AP at normal low venous and capillary filling pressures so that efficient exchange at the capillaries can continue.
At rest these patients have adequate CO and AP with venous capillary pressures low enough to result in normal capillary fluid dynamics or net efflux of small enough quantity that increased lymphatic drainage can compensate.
Clinical signs at this point may include:
Exercise intolerance—“asked” to do more work, the system is unable to maintaining adequate CO and AP at low venous capillary pressures; the patient tires more rapidly and may even decompensate if they attempt to do too much for too long a period of time.
Cough due to physical enlargement of the heart irritating major airways
The “fragile” or symptomatic, decompensated patient:
As severity of the underlying anatomical or functional lesion progresses, compensatory mechanisms may be overcome or become detrimental, and patients decompensate.
Adequate CO and AP, maintained via neuroendocrine stimulation and fluid retention can no longer be achieved at normal capillary filling pressures CHF.
In addition, excessive exposure to catecholamines (arrhythmias, down-regulation of beta-receptors, cardiac fibrosis), aldosterone, angiotensin II (cardiac hypertrophy and fibrosis), etc., may contribute to decompensation.
It is at this point that clinical intervention is, without doubt, needed and beneficial.