Heart failure, by definition, occurs when cardiac output is insufficient to provide the tissues with adequate blood flow and / or when the venous return to the heart is greater than the amount of blood that the heart can expel at normal filling pressure. Most animals with heart failure show signs of both forward and backward failure. Forward failure refers to the inability of the heart to pump sufficient blood forward and the inadequate tissue perfusion which ensues, backward failure occurs when the left and / or right ventricular end-diastolic pressure (preload) increases. This leads to increased venous pressure behind the affected chambers and the development of passive venous congestion of the lungs, liver and other tissues.
Numerous compensatory neurohumoral mechanisms become operative when cardiac output starts to fall. These compensatory changes are entirely appropriate for low output failure caused by circulatory shock, for example hypovolaemic shock, and are designed to maintain cardiac output at a level which is at least sufficient to ensure adequate tissue perfusion when the animal is at rest. If, however, a cardiac abnormality is responsible for the low output then, in the longer term, these compensatory responses become inappropriately regulated to a point that they are detrimental to the animal, further increasing the workload on the heart and setting up a self-perpetuating cycle of ventricular dysfunction. Sustained compensatory mechanisms trigger adaptive changes in the heart and blood vessels leading to further compromise in cardiac function and signs of passive venous congestion. Thus, clinically, signs of low output failure are usually associated with varying degrees of circulatory congestion. The cardiac function curves shown in site demonstrate these two situations of low output failure and congestive failure. Clinical cases can occur anywhere between these extremes and therefore may show a combination of low output and congestive signs depending on the level of activity attempted and the cardiac output required to maintain adequate tissue perfusion.
On a pathophysiological basis heart failure may be divided into four components; myocardial failure, volume overload, pressure overload and compliance failure.
Impaired myocardial contractility leads to systolic dysfunction which is characterized by a reduction in stroke volume and signs of low output (forward) failure. Myocardial failure may be primary (for example cardlomyopathy) or may occur secondary to prolonged volume overload. The myocardial failure which is a feature of dilated cardiomyopathy usually follows a more chronic course and numerous compensatory mechanisms come into operation to counteract the impaired myocardial function and decrease in cardiac output (see section on compensatory mechanisms).
Volume overload (increased preload)
Volume overload results in ventricular dilatation to a point where the ventricle decompensates, that is, myocardial contractility decreases and signs of both congestive heart failure and low output failure occur. Signs of congestive heart failure associated with the regurgitation of blood into the atria and volume overload may occur before myocardial decompensation and it has been shown that myocardial contractility is often normal or only mildly abnormal in dogs with congestive heart failure due to chronic mitral endocardiosis.
Causes of volume overload include the following.
- Atrioventricular insufficiency. Incompetence of the atrioventricular valves leads to regurgilation of blood from the ventricles to the atria. This may be due to endocardiosis, endocarditis, dilation of the atrioventricular annuli as occurs with dilated cardiomyopathy, and ruptured chordae tendineae.
- Left to right cardiovascular shunts which over-load the left side of the heart via the lungs. Examples include patent ductus artcriosus, ventricular septal defect and atrial septal defect.
- Sodium and water retention (see section on compensatory mechanisms).
Pressure overload (increased atterload)
Conditions which cause increased vascular resistance and which impede the ejection of blood through the ventricular outflow tracts result in ventricular hypertrophy.
Causes of pressure overload include:
- Aortic or pulmonic stenosis
- Hypertrophic cardiomyopathy
- Pulmonary hypertension (for example chronic obstructive pulmonary disease, dirofilariasis or pulmonary thrombosis).
- Increase in systemic vascular resistance (for example systemic hypertension associated with chronic renal insufficiency).
Compliance failure implies a loss of myocardial elasticity so that the ventricle is unable to relax and distend properly during diastolic filling. The haemodynamic abnormalities therefore reflect diastolic dysfunction rather than systolic dysfunction which occurs with myocardial failure. Compliance failure may be associated with ventricular hypertrophy, myocardial fibrosis and pericardial effusion (cardiac tamponade).
Extracardiac factors such as excitement, heat stress, overexertion, infection, trauma, anaemia, shock, obesity, pregnancy or any severe systemic or metabolic disease process can also contribute to cardiac decompensation in an animal with preexisting cardiac disease.
Circulatory disturbances can cause similar cardiac dysfunction either by reducing cardiac output or by creating high output states which overload the heart.
Low output states may be caused by:
1. Decreased preload, for example.
- Overzealous use of diuretics and / or vasodilators to treat congestive heart failure
- Hypovolaemia due to haemorrhage or hypoadrenocorticism
- Reduced venous return (for example compression of the posterior vena cava by a large abdominal mass, ascites, gastric torsion)
2. Dysrhythmias (either tachy- or bradydys- rhythmias)
High output states which overload the heart may be associated with:
1. Chronic anaemia, arteriovenous fistulae (for example cardiovascular shunts) and hyper-thyroidism
2. Overzealous administration of intravenous fluids
Mechanisms which moderate these compensatory effects
If the compensatory mechanisms go unchecked their effects on cardiac function would be detrimental. A number of other mechanisms moderate their effects.
Increased atrial stretch by raised atrial filling pressures stimulates the release of atrial natriuretic peptide (ANP) and atrial stretch receptors elicit reflex responses. Both these hormonal and neural reflex responses to stretch tend to limit salt and water retention by the kidney and limit the high vascular resistance against which the heart has to pump. ANP itself inhibits release of noradrenaline from sympathetic nerve endings, reduces secretion of aldosterone and has direct vasodilatory and natriuretic effects. A trial natriuretic peptide (ANP) concentrations in dogs with congestive heart failure increase as much as sixfold. Neural reflexes also reduce traffic in sympathetic nerve fibres and stimulate the release of a non-peptide natriuretic factor from the hypothalamus.
Cardiac muscle hypertrophy occurs, increasing the thickness of the muscular ventricular wall. This tends to reduce wall stress (distributing it among an increased number of sarcomeres) and therefore the work required to raise the tension within the ventricular wall during the isovolumetric phase of systole.
These factors tend to create a delicate balance allowing the compensatory mechanisms to restore cardiac function back cowards normal while, at the same time, ensuring that the cost in terms of myocardiat energy consumption is minimal.
Pathophysiology of heart failure related to the underlying cause
The above pathophysiological scenario is applicable to heart failure in patients regardless of the underlying cause. For example, in myocardial diseases such as dilated cardiomyopathy, the underlying problem is one of poor systolic function. During the chronic stages of this disease, the compensatory mechanisms and adaptive changes referred to above lead to volume overload and congestive signs which may hasten the deterioration of myocardial function.
Regurgitant valvular heart disease and congenital abnormalities causing left to right shunts also cause cardiac volume overload with the same mechanisms attempting to compensate for a reduction in cardiac output. Although cardiac muscle function may be normal in these diseases, prolonged activation of the compensatory mechanisms described above may eventually lead to detrimental effects on cardiac muscle function (cardiomyopathy of overload).
Diseases which affect diasiolic function to reduce cardiac output will also activate the same neurohortnonal mechanisms. Examples include hypertrophic cardiomyopathy and pericardial disease. In the former case, the problem is one of lack of ability of the cardiac muscle to relax and fill properly during diastole and it is characterized by concentric ventricular muscle hypertrophy. Here, expansion of the circulating volume and increased venous return fail to stretch the diseased muscle and circulatory congestion results. With pericardial disease, raised pericardial pressure opposes ventricular filling (particularly of the more compliant right ventricle)- Compensatory changes raising venous return and filling pressure are essential if cardiac output is to be maintained. Fortunately, congestion of the systemic circulation is less life-threatening in its effects than congestion and oedema of the lungs.
Valvular diseases which cause stenosis (aortic and pulmonic stenosis) lead to pressure overload of the respective ventricles. Concentric muscle hypertrophy results from the increased work load encountered in overcoming the obstruction to cardiac output. Such animals usually show signs of syncope on exercise and develop fatal arrhythmias before compensatory mechanisms for poor cardiac output lead to circulatory congestion.
In conclusion, the compensatory and adaptive changes which occur in cardiac failure are the same regardless of the underlying cause. Inappropriate regulation of these mechanisms in chronic heart failure contributes to the self-perpetuating cycle of events leading to cardiac decompensation and signs of both forward and backward failure. For this reason, medical management strategies are aimed at counteracting some of these compensatory and adaptive changes and knowledge of the underlying cause will assist in determining the most appropriate treatment regime.
Cardiac cachexia refers to the severe wasting that occurs in association with chronic congestive heart tail urc. The weight loss which can be rapidly progressive is usually accompanied by lethargy, generalized weakness, inappetence and poor hair coat. Affected animals generally show severe signs of congestive heart failure and are moderately hypoproteinaemic. Cardiac cachexia has been attributed to a combination of factors including poor tissue perfusion, cellular hypoxia, malabsorption and anorexia.