Beginners guide to cardiac pharmacology

Until fairly recently, drugs used in cardiac medicine were limited to treating clinical signs of heart failure as they occurred, or for the management of arrhythmias. However, advances in canine drug therapy mean that patients with heart disease can now be treated before they develop symptoms, thereby prolonging survival time. Drugs used in the treatment of heart disease and failure can be split into three categories depending on their mode of action. They either remove excess fluid, promote cardiac contractility or inhibit the neurohormonal response activated in heart failure. Anti-arrhythmic drugs are divided into those that treat tachyarrhythmias and those that treat bradyarrhythmias. All drugs used in cardiac medicine can have deleterious effects and require routine monitoring; however, anti-arrhythmics have the potential to cause or worsen arrhythmias, and therefore need extra caution and careful observation.

Heart disease is defined as any abnormality of cardiac structure or function. Heart failure is said to occur when clinical signs of increased tissue water and/or decreased tissue perfusion are present. The primary function of the heart is to maintain adequate blood pressure (see Figure 1). If for any reason cardiac output is compromised leading to a fall in blood pressure, two compensatory mechanisms are activated, in an attempt to normalise it (see Table 1). These compensatory mechanisms are the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) (also known as the neurohormonal system). They act by increasing fluid retention, increasing vasoconstriction, and stimulate the heart to increase heart rate, all aimed at improving cardiac output. However, if arterial blood pressure cannot be normalised despite maximal activation of compensatory mechanisms, then low output heart failure will occur. Sometimes the fall in output is so acute that compensatory mechanisms have had insufficient time to activate, which may be seen with some arrhythmias or myocardial infarction. Although life saving in the short term, long-term stimulation of compensatory mechanisms causes progressive deterioration of cardiac function due to fatigue of the heart muscle. Patients can either present in acute life-threatening heart failure or with chronic heart failure. Figure 2 shows a cat open mouth breathing due to acute heart failure. For clinical signs of both, see Table 2.