The cardiac pathologies manifested and that appear in the consultation with pictures of major or minor gravity, are one of the groups of illnesses that with more frequency we can find in the canine clinic every day, though in the feline clinic they lose one of the places of major entity opposite to the respiratory pathologies that turn out to be much more frequent.
Some studies demonstrate that between the dogs that come to a veterinary consultation for some illness, at least 10% presents certain type of cardiac injury with some grade of clinical consistent symptoms, the vaccinations are excluded in this case, deworming, routine periodic checkups. This number supposes that a small hospital that attends every day only up to 5 canine patients, has in the exploration table a patient with some type of more or less serious cardiac and more or less evident injury, every two days.
The clinics that attend a major number of patients, see how this number goes off, especially when it is a question of active files for a long time since the majority of the faithful patients are doing that the average of our file become more and more advanced.
The fact of having on the exploration table a patient with cardiac failure every 2 days in a modest consultation, does not suppose, unfortunately, that we could detect all these patients, to study them, to realize the precise diagnostic tests, to establish a finished and exact diagnosis, to plan a medical-hygiene-nutritional treatment that is followed in a strict form and to know that we will see this patient in all the due follow ups. It turns out evident, nevertheless, that if we are not conscious as veterinarians that our patients present these pathologies and with this theoretical incidence, it will be slightly probable that we achieve that their owners take initiatives for their diagnosis, treatment and periodic control.
Once made this introduction, we have to know that the cardiac injuries can be grouped in a very general form in several types of patients and illnesses, types that do not correspond with academic or theoretical classifications but that is going to be useful as practical approach system to these pathologies:
Degenerative injuries of gradual and slow evolution
Serious injuries of rapid evolution
PHYSIOPATHOLOGY OF CONGESTIVE HEART FAILURE
When for any reason we find a decrease of the cardiac expense, in other words, of the blood quantity that the heart pumps per minute, in an immediate form the pressure recipients are activated at carotid and renal level and the compensatory defense mechanisms are stimulated, which are directed to modify in an immediate way and during short time periods the decrease of the cardiac expense, as well to modify in a permanent way the characteristics of cardiac contraction frequency, arterial pressure, precharge or postcharge, so that the cardiac expense readjusts to the organic needs, and it is achieved finally a new state of balance of cardiac functionality.
One of these first compensatory mechanisms is the increase of the sympathetic tone: a sympathetic stimulation supposes a rapid response to a decrease of the cardiac expense and obtains multiple effects.
It is a very rapid response but only is valid in the short term, allows to face situations of urgency where a high cardiac expense is demanded in a certain moment: struggles, flights, aggressions, wedding stops.
The increase of the sympathetic tone produces, between other effects, the following ones:
1. Increase of the cardiac frequency, it is one of the components of the cardiac expense:
Cardiac expense = Frequency x Volume (in each heartbeat)
Providing that certain physiological maximum limits are not exceeded, to major cardiac frequencies major cardiac expense.
2. Increase of the arterial vasomotor tone: basically an arterial vasoconstriction is achieved which manages to increase the postcharge but also the blood pressure so that this one does not go under certain minimal limits necessary for a good cerebral, renal and cardiac irrigation. The increase of the postcharge supposes an increase of the resistance for the heart to win to pump blood across the arteries, in other words, they increase the requirements in order that the heart develops a certain muscular work that can increase its fatigue.
3. Increase of vascular venous tone, this improves the preload, manages to increase the blood quantity that comes to the right auricle, if we bear in mind that to major distension of the right auricle, major cardiac expense, we are managing to increase the cardiac expense that has been diminished. It is important to remember that also in this case, a maximum tolerable limit exists, if it excels itself, for much that tries to raise the preload, the heart will be unable to obtain a major blood pumping.
4. Renin liberation at the juxtaglomerular renal level, which unleashes the waterfall of renin-angiotensin-aldosterone that we will see further.
5. The contraction of the musculature of the myocardium is improved, other of the factors with great influence in the cardiac expense. If the cardiac muscle has major capacity of contraction, is probable that it becomes more effective on having developed its functions of pumping.
6. As an undesirable and inevitable side effect, the appearance of arrhythmias is promoted by the excessive sympathetic tone; basically tachyarrhythmias, that can be serious, especially if they are of ventricular origin, that it is the most frequent thing in these cases.
7. Also there are other important and harmful effects that appear: increase of the oxygen consumption on part of the myocardium: this concept refers to the quantity of oxygen that the cardiac muscle needs (consumes) to realize a contraction.
The meaning of this situation is that whenever that happens there is an increase of the oxygen consumption from the myocardium, this situation must go accompanied of an increase of the cardiac expense and coronary blood flow (origin of the oxygen contribution to the myocardium), or in the opposite case, the demand of oxygen will be superior to the availability of the same one and the metabolism will prevail anaerobic.
The anaerobic metabolism of the myocardium supposes in an immediate way a minor efficiency in the myocardic work (rapid decrease of the contractions) and frequent appearance of cardiac arrhythmias that can generate a major decrease of the cardiac expense and a new decrease of the coronary blood flow, closing a vicious circle that tends to worsen on a gradual form the hemodynamic situation.
The increase of the sympathetic tone, is accompanied by the sympathetic stimulation of intrarenal recipients as of juxtaglomerular baroreceptors.
The juxtaglomerular apparatus is a complex system of detection, regulation and control, capable of detecting several factors; the dense macula is a group of specialized cells considered as local chemoreceptors, besides in the same juxtaglomerular apparatus, exist beta-adrenergic recipients and also have been identified alpha-adrenergic recipients.
The second mechanism of protection is the renin-angiotensin system that is activated across the sympathetic activation that we have already seen and in a direct form when the juxtaglomerular apparatus detects a decrease volume or the pressure of the afferent blood in the glomerular arteriole.
This second system is slower in its restoration but it manages to control longer term situations so that it constitutes the "second line of defense" in front of slower development problems than the ones compensated by the already described sympathetic activation.
When this second detection system is activated, the immediate response is the RENIN liberation, an enzymatic factor that is liberated to the circulating blood, where it acts on an ALPHA-2-GLOBULIN: THE ANGIOTENSINOGEN, which for the enzymatic action of the renin, transforms in ANGIOTENSIN I, which is an inert molecule without any biological action.
The RENIN is a proteolytic enzyme of a molecular weight of approximately 40,000 that joins its substrate, the angiotensinogen, to act liberating the angiotensin I.
The ANGIOTENSIN I, it is an inactive decapeptid, of approximate molecular weight of 1,300 and is located in the circulating blood, is necessary for it to suffer the enzymatic action of the ANGIOTENSIN CONVERTING ENZYME (A.C.E.), formed in vascular tissues, reason for which it is very abundant in the pulmonary parenchyma.
Thanks to this new enzymatic action, the angiotensin I transforms into an octapeptid, biologically active and that has been named previously HYPERTENSIN or ANGIOTONIN, now, named ANGIOTENSIN II, with a very short half-life, but it is the most powerful vasoconstrictor known and that has multiple biological actions, some of which still are slightly well-known, but between them we have the following ones:
1. It produces an intense constriction of the peripheral arterioles: in other words, we obtain a strong increase of the cardiac postcharge. This action is achieved thanks to an intense contraction of the vascular walls and it is about an intense selective action in: kidney, spleen and skin and less intense in the central nervous system, the skeletal muscle and the own heart. With this effect, it is achieved an increase of the vascular peripheral resistance and consistently an increase of the average blood pressure.
2. It also takes place a constriction of the renal arterioles; basically it is a question of protecting the renal function.
3. Also, it takes place a moderate constriction of the peripheral veins; what is achieved is an important increase of the preload, with which, the tendency is to increase the cardiac expense.
4. Also the liberation of ALDOSTERONE is stimulated; basically there is an increase of the production and liberation of organic steroids, between which are the mineralocorticoids and between them the aldosterone, that is a steroid hormone of molecular weight of 360.4, secreted by the glomerular zone of the adrenal cortex and, undoubtedly, it is the most powerful regulator of the electrolytes excretion. The ALDOSTERONE, has several actions:
Increase of the renal retention of sodium with a developing secretion of POTASSIUM and HYDROGEN ions in the light of the renal tube. The reabsorption of sodium and chlorine tends to increase the osmolarity of the extracellular liquid, which facilitates the liberation of the ANTIDIURETIC HORMONE (ADH) that improves the renal retention of water.
Increase of ADH liberation; that originates a major water renal retention.
With these two points, we obtain a combined water and sodium retention, in other words, an increase of the circulating volume, this way it is accomplish to increase the blood pressure, the precharge and the postcharge.
The ANGIOTENSIN II has an short half-life since the ANGIOTENSINASES of tissular origin and present in the plasma, principally the ANGIOTENSINASE A or AMINOPEPTIDASE and the ANGIOTENSINASE B or ENDOPEPTIDASE, metabolize the angiotensin II, forming several inactive fragments and an HEPTAPEPTIDIC ACTIVE fragment that is a molecule that is starting to be named ANGIOTENSIN III and supports some biological actions, principally a powerful action on the liberation of aldosterone.
The same enzyme that catalyze the step of angiotensin I to angiotensin II, in other words, the A.C.E., it is also responsible for the inactivation of the vasopressure hormone BRADIQUININE, for this reason, in occasions it has been named KININASE II to the A.C.E., in other words, in addition to the seen, it annuls a physiological mechanism of vasodilatation, again, we will have one more factor that helps to raise the blood pressure to preserve organic vital territories with a minimal cardiac expense.
These defense systems are compensated by the existence of other antagonistic mechanisms that are based on the existence of the atrial natriuretic peptide (ANP), a real cardiac hormone that is synthesized in the right auricle and that is liberated to the circulating blood when on this right auricle an overfilled stimulus is detected, once in the peripheral blood, it exercises a hypotension action; it reduces the circulating volume due to the increase of the renal excretion of sodium and to the increase of the capillary permeability.
It is also suspected, that antagonizes the action of the angiotensin II diminishing sodium and water retention.
The levels of ANP increases in the cases of tachycardias and in the cases in which it appears a serious decrease of the cardiac expense.
Together with the ANP, the existence of another natriuretic hormone has been detected: the Sodium active transportation inhibitors. Probably these hormones originate in a set of specific adjacent areas of the brain to the third ventricle implied in the regulation of the volume and concentration of the extracellular liquid.
When these mechanisms that manage to increase the circulating volume and to modify the blood delivery towards organs that are very sensitive to the hypoxia, are kept during long periods of time without been modified, undesirable effects takes place since it puts under an obligation to an injured heart to realize a constant and more intense additional effort, if the cause that unleashed the whole process is not eliminated, finally it takes place a cardiac depletion and the incapability of the same one to face less awkward situations, appearing heart failure symptoms in front of the most minimal demands of cardiac expense increase.
TREATMENTS OF CONGESTIVE HEART FAILURE IN COMPANION ANIMALS. VASODILATORS AND SODIUM RESTRICTION IN THE DIET
The patients with congestive heart failure start by retaining a superior quantity than the normal one of sodium, even before demonstrating clinical symptoms of the cardiac process or of its physiopathologic consequences, really the capacity of retention or of elimination of sodium, can be used as indication of congestive heart failure.
A diagnosis of the cardiac illness allows to value the possibility of restoring an adequate drug treatment or a moderated restriction of sodium as precocious measure and almost prophylactic treatment. In the patients with initial phases of congestive heart failure in which we restore this restriction, they stop the sodium retention and the consecutive liquid retention.
When the cardiac illness is more advanced, in addition to the decrease of the ingested quantities of sodium, it will be necessary to restore a more finished medical treatment to compensate the clinical situation.
In many occasions, the patients do not come to the hospital until they are presenting a congestive heart failure in the IInd or IIIrd phases and the general rule is that from the IInd phase is necessary to restore, not only a diet treatment, but also a medical treatment.
The medical therapy will depend in a very important way of the primary cause of the cardiac illness that originates the insufficiency, habitually and in different combinations, the following pharmacological groups are used:
All the previous groups of medicines, enter in what we might consider specific or complementary therapeutics of the congestive heart failure and constitute a very extensive and varied arsenal that is complicated as for its possible uses with the infinite combinations of two, three or more of these medicines used in complex treatments in a long term, in patients of advanced age and not always with a good function of other organs or systems, being in many occasions more or less important shortcomings of hepatic or renal function that will interfere in a notable way in the metabolism, activity, half-life or elimination of the medicines that we use.