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 volume or end‐systolic pressure.
The volume or pressure in the left ventricle is generally used to determine preload.
It is dictated in large part by venous return.The venules serve as capacitance vessels or reservoirs, storing the majority of the circulating blood volume. They constrict during times of increased demand, thereby increasing venous return and preload. The great veins and the spleen also act as reservoirs for blood.Anesthetic drugs that can change venous return include acepromazine (via vasodilation) and alpha2 agonists (via vasoconstriction).Venous return is affected by a number of factors including circulating blood volume, body position, phase of respiration and respiratory disease (due to changes in intrathoracic pressure) and valvular regurgitation.
Ideally, an appropriate preload will cause stretch of the myocardium, which will improve contractility and increase SV due to Frank‐Starling's Law of the heart (see Table 3.1).
Afterload
Is the pressure or resistance against which the ventricle must pump in order to eject blood.
Although aortic impedance is the most accurate measurement, arterial BP is the most commonly used index of afterload. (see section on BP for more information.)Aortic impedance = Aortic pressure/Aortic flow.
End‐systolic ventricular wall stress is also used to describe afterload.At the end of systole, with the aortic valve open, increased resistance in the vascular system will be imposed on the ventricles and will increase ventricular wall stress.
Anesthetic drugs that can affect afterload include acepromazine (vasodilation decreases afterload) and alpha2 agonists (vasoconstriction increases afterload).
Contractility (inotropy)
Defined as the ability of cardiac muscle fibers to shorten or develop tension.Cardiac muscle contraction is initiated by an action potential which triggers the release of intracellular calcium and the flux of extracellular calcium into the cell, ultimately resulting in cross bridging of actin and myosin and a shortening of the sarcomere.
Ejection fraction is a simple measurement of contractility.Ejection fraction is the ratio of the SV to the end‐diastolic volume.Normal ejection fraction is 60–70%.
Other indices used to evaluate contractility include the rate of change of ventricular pressure with respect to time (dP/dt), ventricular function curves, and pressure‐volume loops.
Increased contractility causes an increase in myocardial oxygen consumption.
Factors that affect contractility include:Autonomic tone.Acidosis, hypoxia.Thyroid disorders.Electrolyte imbalance.Anesthetic drugs.
Anesthetic agents that affect contractility include:Barbiturates, propofol and inhalant anesthetic gases cause a decrease in myocardial contractility.Ketamine causes an indirect increase in myocardial contractility via stimulation of the sympathetic nervous system (the direct effect of ketamine is decreased contractility).
Relaxation (lusitropy)
Corresponds to the extrusion/reuptake of calcium and relaxation of the sarcomere.
Imperative for normal diastolic function.
Impaired by conditions like hyperthyroidism and heart failure, and by anesthetic drugs such as most inhalational anesthetics.
D Blood Pressure (see Table 3.2)
Although cardiac output is a more precise measure of cardiovascular function, BP is easier to measure and is often used for evaluation of the cardiovascular system. (See Chapter 19.)
BP = Cardiac output (Q) × Systemic vascular resistance (SVR) Note: SVR is often referred to as total peripheral resistance (TPR).
Pulmonary vascular resistance (PVR)
Arterial BPs are recorded as systolic, diastolic and mean values.Systolic pressure = Peak pressure.Diastolic pressure = Nadir pressure.Mean pressure = 1/3 (Systolic pressure − Diastolic pressure) + Diastolic pressure.
Reference values in conscious adult horses are:Systolic pressure of 147–169 mmHg.Diastolic pressure of 92–110 mmHg,Mean pressure of 115–131 mmHg.
These values should be maintained at not lower than a 40–50% decrease in the anesthetized horse.
E Physics of flow
Blood in the middle of the vessel flows freely, whereas it flows slowly at the periphery because of the friction with the endothelium.In a small vessel, a large percentage of the blood is in contact with the vessel wall so the rapidly flowing central stream is absent.
Although capillaries have the smallest vessel diameter, arterioles pose the highest resistance to blood flow (i.e., there is greater perfusion pressure drop across the arterioles than across any other segment of the systemic circulation).Due to the fact that each arteriole distributes blood to numerous capillaries, thus making the net resistance of the capillaries less than the resistance of the single arteriole delivering blood to them.Thus, dilation and constriction of the arterioles dictates organ and tissue blood flow.
