Page 440 - Clinical Small Animal Internal Medicine

408 Section 5 Critical Care Medicine

of oxygen delivery (DO 2 ). In fact, only seven parameters for diagnosing a patient in shock. Heart rate can be
VetBooks.ir can be manipulated to augment oxygen delivery: those manipulated pharmacologically with beta‐2‐adrenergic
agonists and anticholinergic drugs. However, the ability
associated with cardiac output (heart rate, preload [end‐
diastolic volume], afterload [MAP], systemic vascular
ited. Diastolic filling time is essential for preload and
resistance, and ejection fraction), and those associated of changes in heat rate to improve cardiac output is lim­
with arterial oxygen content (hemoglobin concentration tachycardia shortens the amount of time spent in dias­
and partial pressure of inspired oxygen). tole during the cardiac cycle. At very high heart rates,
this shortened diastolic time can significantly decrease
preload and cardiac output. Patients in the decompensa­
Cardiac Output
tory stage of shock can become absolutely or relatively
Cardiac output is determined by the amount of the blood bradycardic as the heart begins to fail due to poor oxygen
ejected from the heart with each beat (stroke volume) delivery to the heart itself.
and the rate at which the heart is beating (heart rate).
Stroke volume, in turn, is determined by the amount of Arterial Oxygen Content
blood that returns to the heart (preload), the force that
must be overcome to eject blood out of the heart (after­ Oxygen content of the blood is the sum of the oxygen
load/systemic vascular resistance), and the physical force dissolved in the blood (PaO 2 ) and the amount of oxygen
that the heart must generate to move blood (contractility that is bound to hemoglobin. The amount of oxygen
or inotropy). Cardiac output is arguably the easiest com­ bound to hemoglobin is a much more important con­
ponent of DO 2 to manipulate. Accordingly, increasing tributor to total blood oxygen content while PaO 2 is a
preload is the most common initial treatment of shock more important indicator of the lungs’ ability to oxygen­
and is accomplished with the administration of IV fluids ate the blood.
and vasoactive medications to augment preload by Interventions directed at improving arterial oxygen
increasing venous pressure and consequently right ven­ content include provision of supplemental oxygen
tricular volume. (increasing PaO 2 ) and transfusion of hemoglobin in
The heart has the ability to increase or decrease the the form of red blood cells or hemoglobin‐based oxy­
force of contraction (inotropy) exerted during systole. gen carriers (increasing oxygen‐carrying capacity).
Intrinsically, the heart pumps more powerfully when The importance of hemoglobin concentration in oxy­
there is a larger amount of blood present in the ventricle gen delivery cannot be overstated. Hemoglobin makes
at the end of diastole (Starling law of the heart). the transport of oxygen in the blood and subsequent
Sympathetic stimulation can also increase the force of offloading at the tissue bed much more efficient.
contraction and is in fact the primary mechanism by Consequently, raising hemoglobin is the best way to
which inotropy can be altered by the clinician through improve arterial oxygen content if lung function and
administration of beta‐1‐adrenergic agonists. ventilation are normal. Supplementation of oxygen to
The impediment of flow that must be overcome to those patients who are normoxic (have a normal PaO 2 )
eject blood out of the heart is the systemic vascular will do little to increase the amount of oxygen pre­
resistance (afterload). This is the force that the cardiac sented to the tissues (assuming the supplementation is
wall is placed under when it contracts in systole and is at normal atmospheric pressure) when compared
usually considered as the mean arterial blood pressure to supplementation of hemoglobin. Consider a dog
(MAP). Although convenient, this is not always accurate. breathing room air; assuming a hemoglobin concen­
As an example, MAP and afterload are uncoupled when tration of 6 g/dL (HCT 18%), PaO 2 of 90 mmHg, and
an anatomic obstruction to flow exists, such as subaortic arterial hemoglobin saturation (SaO 2 ) of 95%, the cal­
stenosis. Manipulation of afterload (SVR and MAP) is culated CaO 2 would be 8.0 mL O 2 /dL. By increasing
possible through the administration of agents acting on the fraction of inspired oxygen to 40%, the resultant
specific vasoactive receptors (alpha, dopamine, and vas­ CaO 2 would increase to 8.55 mL O 2 /dL for an 8%
opressin). Most frequently, the goal is to increase both increase. Now assume raising the hemoglobin with no
SVR and MAP. Afterload reduction is infrequently a con­ oxygen supplementation. By increasing the hemo­
cern in veterinary patients although it is common in globin concentration to 9 g/dL (HCT 28%), a CaO 2 of
humans due to that species’ propensity for developing 12 mL O 2 /dL can be achieved for a 54% increase. In
primary hypertension. order to extract the most benefit from an increase in
Heart rate changes are important for the second‐to‐ hemoglobin concentration, it must be maximally satu­
second adjustment of cardiac output. During shock, rated with oxygen so oxygen supplementation is always
increases in heart rate typically parallel increases in inot­ warranted during shock to ensure the highest possible
ropy. Clinically, heart rate measurement is a useful tool PaO 2 is achieved.