The audible “cardiac impulse” or “apex beat” occurs during early systole when the contracting heart twists slightly, causing the left ventricle to strike the chest wall just caudal to the left olecranon.A “c” wave will be observed during early systole due to bulging of the tricuspid valve into the right atrium or possibly due to pulsations from the carotid artery.Ventricular contraction causes the atria to collapse toward the ventricles (ventricular “suction”), which causes a brief collapse of the jugular vein and a decrease in atrial pressure (the “x” descent).
Following this event, atrial filling begins.This generates the positive “v” wave.
C Events occurring at the end of the ejection period (late systole/early diastole)
Ventricular pressure rapidly drops below the pressure in the aorta and pulmonary artery, causing a reversal of the direction of blood flow and closure of the semilunar valves.This produces the high‐frequency second heart sound (S2).In horses, the pulmonary valve may close either slightly after or slightly before the aortic valve, resulting in an audible “splitting” of S2. This splitting is normal but can be dramatic in horses with pulmonary disease.Along with aortic recoil, valve closure produces the incisura of the arterial pressure curve.
Comment: The volume of blood ejected during systole is called SV, and the ratio of the SV to the end‐diastolic volume is the ejection fraction, which is a commonly used measure of systolic function.
D Events occurring during early diastole
Ventricular pressure continues to fall with no change in ventricular volume (isovolumetric relaxation).
This proceeds until the ventricular pressure drops below atrial pressure, when the AV valves open and the phase of rapid ventricular filling begins.Ventricular pressure rises slowly but ventricular volume increases rapidly as blood that accumulated in the atria during ventricular systole flows rapidly into the ventricle.Rapid filling may be associated with a functional protodiastolic murmur and the termination of rapid filling results in the low‐frequency third heart sound (S3).The rapid decline in both atrial volume and pressure results in the “y” descent on the atrial pressure curve and may be visualized as a collapse of the jugular vein.
The period of rapid ventricular filling is followed by a period of low velocity filling (diastasis) which extends until the next atrial systole.In the resting horse with a normal HR, diastasis is the longest period of diastole.During diastasis, jugular vein filling may occur, especially during periods of bradycardia.
SA node firing followed by atrial contraction occur during the last phase of ventricular diastole and start the cardiac cycle again.
VI Cardiovascular function and clinical applications
Clinically, cardiovascular function is determined by measurable components such as HR, blood pressure (BP) and cardiac output (see Table 3.2).
Anesthetic drugs, surgical positioning, surgical events (e.g. hemorrhage) and pathology prior to surgery (e.g. sepsis) can have a profound effect on cardiovascular function.
A Cardiac output
Defined as the volume of blood ejected by the ventricles per minute (l/min).
Equals the product of HR (beats/min) and SV (l/beat).
In a normally functioning heart, cardiac output equals venous return.
Cardiac output in the conscious resting horse (400–500 kg) is 32–40 l/min.
To standardize cardiac output among individuals, it is often normalized for body surface area or body weight and reported as cardiac index.Cardiac index in the conscious, resting horse is 70–90 ml/kg/min.
Factors affecting cardiac output:
HR.
Preload.
Afterload.
Contractility.
B Heart rate
Horses have a wide HR range.A resting rate of 24–50 beats/min to a high of 220–240 beats/min at exercise.
Increased HR will generally result in increased cardiac output if SV is constant.In horses, the greatest changes in cardiac output generally occur due to a change in HR (rather than in SV).Table 3.2 Summary of formulas for cardiovascular variables.NameFormulaCardiac output (Q)Heart rate × Stroke volumeMean arterial blood pressureCardiac output × Systemic vascular resistanceSystemic vascular resistance (SVR)Pulmonary vascular resistance (PVR)Arterial oxygen content (CaO2)Oxygen delivery (DO2)CaO2 = ([Hb] × SaO2% × 1.36) + (PaO2 × 0.003)Cardiac output × arterial oxygen content
Extreme tachycardia may actually decrease cardiac output because diastolic filling time is decreased, resulting in decreased SV.
Extreme tachycardia can cause arrhythmias and worsen cardiac disease since the rapidly beating heart spends less time in diastole, the period of the cardiac cycle in which the myocardium is perfused.
During tachycardia, myocardial oxygen delivery is decreased at a time when myocardial oxygen consumption is increased, resulting in inadequate oxygen delivery to the myocardium (i.e. oxygen debt).
Factors influencing HR:
HR is primarily regulated by autonomic input.Parasympathetic (decreases) and sympathetic (increases) HR.Horses have inherently high vagal tone which contributes to the slow HR and normally occurring intermittent second‐degree AV block.
HR is also affected by factors such as ambient temperature, body temperature, exercise, pain, fever and anemia, and reflexively controlled by BP through baroreceptor responses.
Various other activities affect HR.For instance, the Bainbridge reflex is an increase in HR secondary to increased right atrial volume and stretching of the SA node.
Anesthetic drugs can affect HR either directly or indirectly.Anticholinergics (e.g. atropine) decrease parasympathetic tone and increase HR.Alpha2 agonists (e.g. xylazine) decrease HR via direct effects on the SA node and indirect effects via the baroreceptor response.Alpha2 agonists cause vasoconstriction and hypertension.Acepromazine and inhalant anesthetic gases may cause hypotension, which can, in turn, cause a baroreceptor‐mediated increase in HR.
C Stroke volume (SV)
Defined as the volume of blood ejected by the ventricles per beat.
SV is the product of preload, afterload and contractility (inotropy).These components are interlinked and interdependent.
Preload
Is the force acting to stretch the ventricular fibers at the end of diastole.
It may be described as either end‐systolic