Shock1; articles cards 26-41 Flashcards
Calculate volume needed for blood transfusion?
Bloodneeded(ml)=
weight(kg)xDesiredPCV−RecipientPCV
_______________________
Donor’sPCV
Then multiply that number ×70(cat)or90(dog)*
Note: A rough estimate is 2.2ml of blood/kg of body weight increases the recipient’s PCV by 1%.
FAST (Focused Assessment With Sonography for Trauma) Protocol to Detect Free Abdominal Fluid in Dogs
Uses two ultrasonographic views (transverse and longitudinal) for what four regions of the abdomen?
Also included is the conclusion made by Lisciandro jvecc 2009
1Subxiphoid region
2Midline position over the bladder
3Right flank in right and left lateral recumbency, caudal to ribs
4Left flank in left and right lateral recumbency, caudal to ribs
Lisciandro 09: Initial and serial AFAST (A=abdominal) with applied AFS (abdominal fluid scoring) allowed rapid, semiquantitative measure of free abdominal fluid in traumatized patients, was clinically associated with severity of injury, and reliably guided clinical management. Where possible, AFAST and AFS should be applied to the management of blunt trauma cases.
Shock dose for animal with severe pulmonary, cardiac, or renal dz?
one-quarter to one-half the calculated shock dose is administered over 15 to 30 minutes, and the patient is carefully reassessed for changes in vital signs.
Oxygen delivery equation? DO2 = …
DO2 = CO x CaO2
Cardiogenic shock?
results from inability of heart to propel blood through circulation; can be interference with diastolic filling or with the ability to pump (systolic failure). Also can be extracardiac like compression of heart or great vessels by some other pathology (sometimes referred to as obstructive shock as its own category)
hypovolemic shock?
inadequate circulating volume causing decreased preload, thus reduced CO
Distributive shock?
impairment of the mechanisms regulating vascular tone, with maldistribution of the vascular volume and massive systemic vasodilation. Decreased systemic vascular resistance causes “relative” hypovolemia and reduction in venous return. (ie sepsis, SIRS, anaphylactic reactions, or neurogenic shock caused by severe damage to CNS with loss of autonomic stimulation on vessels.
Hypoxic Shock?
inadequate arterial oxygen content of cellular oxygen utilization. Most common causes are anemia (reduced hemoglobin concentration–anemic hypoxia), and hypoxemia associated with respiratory failure
Equation for cardiac output….CO = …?
CO = SV x HR
3 factors that determine stroke volume (SV)?
preload, afterload, and contractility
Preload?
Load imposed on a resting muscle to stretch it to a new length. Preload = End Diastolic Volume; An increase in End Diastolic Volume augments the strength of cardiac contractions (Frank-Starling mechanism). Factors that influence preload: splenic contraction, retention of Na and H2O, and increased thirst
Afterload?
The force that opposes muscle contraction, and in cardiac muscle, it is equivalent to the ventricular wall tension developed during systole. Afterload= “pressure in the left ventricle required to eject blood into systemic circulation”
Afterload is influence mainly by ___ ____ ____.
systemic vascular resistance. Low BP is the major determinant of decreased afterload.
Contractility?
the force and velocity of cardiac muscle contraction
Arterial Oxygen Content (CaO2) Equation?
CaO2 = Hb x SaO2 x 1.34 + PaO2 x 0.003*
Thus, oxygen content depends mainly on Hb concentration and oxygen saturation of Hb in arterial blood (SaO2; measured as %).
(*oxygen solubility coefficient)
SaO2 is the percentage of available hemoglobin that is bound to ____?
oxygen
Hb affinity for oxygen increases as oxygen saturation of Hb increases. Thus the oxygen-hemoglobin dissociation curve, which relates Hb saturation of O2 to the partial pressure of O2 (PaO2), is a _______curve.
sigmoidal
What are the 4 factors that influence Hb affinity for O2?
pH, temperature, 2,3-DPG (diphosphoglycerate), and CO2 that can cause a shift in the dissociation curve (ie - making O2 more or less readily released in tissues.
For a normal O2 tension of ___ to ___ mm Hg, the Hb saturation is 100%.
90-100 mm Hg
Describe whether an increase or decrease in each of the factors below causes the O2 disassociation curve to shift to the LEFT (ie. delivery of LESS Oxygen). pH: temp: 2,3 DPG: CO2:
Shift to the LEFT (ie. delivery of LESS Oxygen). pH: Increase temp: Decrease 2,3 DPG: Decrease CO2: Decrease (Note that pH is the only factor that causes a LEFT shift when it is INCREASED)
According to the American College of Surgeons hemorrhage classification system (Box 6-2), loss of ___________ % of circulating blood volume is able to trigger shock, and loss of more than ___________ % of circulating blood volume, if left untreated, induces irreversible shock.
30-40% triggers shock; 40% - irreversible shock
Catecholamine-resistant vasodilatory shock is characterized by refractory hypotension despite intravascular fluid resuscitation and catecholamine administration. Catecholamine-resistant vasodilation is caused by derangements of normal vasodilatory and vasoconstrictor mechanisms, and occurs despite increased levels of norepinephrine, endothelin, and angiotensin II. Author Silverstein (jvecc 2012) found that in dogs with vasodilatory shock that were nonresponsive to dopamine that this drug was effective at increasing blood pressure.
Silverstein found that exogenous
AVP can act as a potent vasoconstrictor in dogs with refractory vasodilatory shock.
AVP = Arginine Vasopressin, aka antidiuretic hormone.
What is AVP aka ADH? Made? Stored?
When is it normally released?
AVP is a potent vasoconstrictor peptide, synthesized in the hypothalamus and stored in the posterior pituitary. Normally, it is released into the circulation in response to an increase in the serum osmolality (sensed in the brain) or a reduction in plasma volume (sensed by baroreceptors in the left atrium, aortic arch, and carotid sinus)
MOA of AVP (arginine vasopressin)
The cellular effects of AVP are mediated by interactions
of the hormone with 2 principal types of receptors:
V1 and V2. V1 receptors, previously known
as V1a receptors, are predominantly located in the gastrointestinal tract and vascular smooth muscle, and
these receptors primarily mediate the vasoconstrictive
response to the hormone. In addition, when present in
high concentrations, AVP causes the HR-arterial pressure
baroreflex curve to shift leftwards by interacting
with V1 receptors in the brain. In contrast, V2 receptors
are primarily found in the principal cells of the
renal cortical and medullary collecting ducts, and these
receptors primarily mediate the antidiuretic effects of
the hormone. AVP also blunts the accelerated synthesis
of nitric oxide following LPS and IL-1b stimulation
in sepsis, and also reduces the vasodilatory effects of
nitric oxide, thereby preventing the nitric oxide-mediated
vasodilation that occurs in sepsis
