Ch 6 Shock Flashcards
Shock
How associated with oxygen delivery (DO2)?
observed when tissue oxygen delivery or utilization is compromised > result sin tissue hypoxia
Oxygen delivery (DO2) depends upon adequate cardiac output (CO) and arterial oxygen content (CaO2).
compensatory mechanisms (4)
(1) tachycardia (to increase oxygen delivery)
(2) tachypnea (to increase oxygenation),
(3) peripheral vasoconstriction (to maintain perfusion of vital organs),
(4) mental depression (in response to decreased perfusion or hypoxia).
4 main types of shock
Hypovolaemic - Reduction in circulating intravascular volume (reduced CO)
Haemorrhage, Burns, 3rd space, dehydration, V+D+
Cardiogenic - Inability of heart to propel blood through circulation. Includes obstructive shock by decreasing to preload
CHF, tension pneumo
Distributive - Maldistribution of vascular volume and massive vasodilation resulting in relative hypovolaemia. Sepsis and SIRS, anaphylaxis, drugs, severe CNS damage
Hypoxic - Adequate perfusion but inadequate arterial oxygen content or cellular oxygen utilisation
DO2 = CaO2 x CO
factors determining oxygen delivery
arterial oxygen = hemoglobin.
ability to carry oxygen ~ the amount of hemoglobin.
saturation ~ function of the hemoglobin molecule + gas exchange in the lung
CO
SV = preload, afterload, and contractility.
CO = SV x HR
Increase heart rate
preload = load imposed on a resting muscle to stretch = EDV
Afterload = force that opposes muscle contraction = pressure during systole, influence by SVR
Contractility = force and velocity
Arterial Oxygen Content
Depends on hb what?
depends mainly on hemoglobin concentration and oxygen saturation of hemoglobin in arterial blood (SaO2)
hemoglobin affinity for oxygen increases as the oxygen saturation of hemoglobin increases)
What factors influence the affinity of Hb for Oxygen
pH, temperature, 2,3-DPG, CO2
what impairs O2 delivery?
reduction in cardiac output > ain determinant of tissue perfusion
Dysrhythmias
preload, afterload, and contractility
Example of a reduction in preload is hemorrhagic shock
decreased afterload is the primary mechanism that leads to distributive shock.
ALTS (Advanced Trauma Life Support) classed of haemorrhage
4 classes
Class 1 - loss of up to 15% blood volume. Clinical signs absent or mild
Class 2 - Loss 15-30%. Tachycardia, tachypnoea, weak pulses
Class 3 - Loss 30-40%. mms pale, CRT prolonged, arterial hypotension
Class 4 - Loss of >40%. Severe and immediately life-threatening. Cold extremities, altered mentation, profound hypotension
Oxygen uptake (VO2)
central venous oxygen saturation normal but tissue oxygenation impaired
Diffussional shunting - slow blood velocity cause diffusion of oxygen from arterial into venous blood instead of into the tissues (in GIT during shock)
Diffusional resistance - Tissue oedema increases diffusion distance and limits oxygen availability
AV shunting - Loss of capillary bloodflow due to SIRS/sepsis, thrombi etc
Perfusion/metabolic mismatch - increased metabolic oxygen demands
Cytopathic hypoxia - mitochondrial dysfunction such as in sepsis
lactate
hypoxia leads to anaerobic glycolysis
if the hypoxia is global, lactate will diffuse into the bloodstream. Major sources of lactate are muscle and the gastrointestinal tract.
compensatory response
shift of body fluids from the interstitium into the intravascular space, augmenting the circulating volume. This compensatory mechanism is a major reason for the observed decrease in total protein level and hematocrit
to support vital organs with adequate oxygen delivery
Maintaining mean circulatory pressure (circulating volume and pressure)
* Maximizing cardiac performance
* Redistributing perfusion
* Optimizing oxygen unloading
reduce BP > reduced baroreceptor and reduced kidney perfusion
stimulates sympathetic system and RAAS
leads to release of adrenalin/vasocontriction and increased volume (Na+ retention) + increased HR > increased CO + SVR
hypothalamic-pituitary-adrenal axis > Cortisol, along with growth hormone, shift in metabolism toward a catabolic state
blood flow is selectively redirected toward vital organs
expense of cutaneous and splanchnic circulation > clinical signs: pale mucous membranes, increased capillary refill time, and cool extremities.
shock also trigger inflammatory responses through hypoxia
cell death dt energy fail > DAMPS released > pro-inflamm.
hypoxia-inducible factors
reintroduction of oxygen to previously hypoxic or ischemic tissues
reperfusion injury is associated with the generation of damaging oxygen and nitrogen free radicals
> auses tissue damage and the release of increased numbers of cytokines and other inflammatory mediators. Neutrophils and endothelial cells are activated, further amplifying the damage and obstructing capillaries
hypoperfusion and inflammation
hypothermia
tissue trauma and promotes an anticoagulant and hyperfibrinolytic state
Proinflammatory cytokines > may directly activate platelets, causing a systemic procoagulant effect
Hypothermia is common in advanced stages of shock and inhibits platelet aggregation
acute coagulopathy of trauma
3 x hypothesis
A fibrinolytic variant fo DIC
Enhance thrombomodulin-thrombin protein C pathway
(decreased thrombin degradation and increased activation of anticoagulant and profibrinolytic protein C)
Neurohumoral response (Catecholamine induced glycocalyx damage and expression of prothrombotic phenotype. Counterregulatory increase in anticoagulants and fibrinolytics leads to systemic anticoagulation and hyperfibrinolysis
What are considered the shock organs in the dog and cat?
dog - GIT
cat - Lungs
Over what MAP ranges will perfusion be maintained to the kidneys, myocardium and the brain?
Kidneys - 70-130mmHg
Myocardium - 60-140mmHg
Brain - 50-180mmHg
What is considered physiologic central venous pressure for dogs and cats?
0-5cmH20
CS
extremely high heart rates, primary rhythm disturbances (e.g., supraventricular tachycardia
rom pale pink to white or gray)
capillary refill time (markedly increased). Limb extremities become cool.
Persistent hypoperfusion leads to various signs of multiple organ dysfunction such as profound mental depression, marked decrease in urine output, and gastrointestinal signs of ileus, diarrhea, and melena.
bacterial translocation and potentially sepsis.
BP = CO X SVR
minimum blood pressure needed to maintain perfusion of major body systems is typically defined as mean arterial pressure > 60 mm Hg or systolic arterial pressure > 90 mm Hg.
patients with hypotension or arrhythmias, the oscillometric method has been reported to consistently underestimate blood pressure
Central venous pressure, in the absence of vascular obstruction, is closely correlated with right atrial pressure. Right atrial pressure is in turn related to right ventricle end-diastolic volume (EDV),
direct and indirect BP monitoring
lactate
normal below 2.5 mmol/L
Evaluating lactate clearance or trends in lactate through sequential blood samples appears to be more useful than obtaining a single value.
a persistently elevated lactate concentration despite fluid resuscitation is indicative of a poor prognosis
Lactate is a late and insensitive marker of hypoperfusion and rises only after the oxygen extraction of tissues has been already maximized
Type A and B lactic acidosis
Inadequate oxygen delivery is the most common cause of increased blood lactate concentration (type A lactic acidosis),
normal oxygen delivery (type B lactic acidosis). occur when mitochondrial function is impaired > sepsis, diabetes mellitus, and neoplasia or drugs and toxins.
monitoring
us: AFST/TFAST
ECG
blood gas
PCV/TP
pule Ox
BP + CVP
Temp
Measurements of cardiac output, blood pressure, lactate concentration, and base excess reflect global perfusion status.
Rectal temperature
Gastric tonometry
Sublingual capnometry
Near-infrared spectroscopy
Pulse oximetry and arterial blood gas analysis are two techniques that allow reliable measurement of oxygenation.
accuracy affected by vasoconstriction, hypothermia, or peripheral hypoperfusion, pigmented mucous membranes
normal SpO2 > 97%
Normal PaO2 is > 90 mm Hg
For patients with supplemental oxygen, the PaO2 should be approximately five times the percent of inspired oxygen (the PaO2/FiO2 ratio should be approximately 500
Treatment
o Initial stabilization should focus on airway, breathing, circulation, and neurologic derangements
o Pathway specific interventions
Optimization of oxygen delivery and reestablishment of adequate tissue perfusion
Aggressive support of organ function
Identification and treatment of the underlying/initiating disease
O2
flow by FiO2 (e.g., 25% to 40% with a flow rate of 2 to 3 L/min)
Mask 1 to 5 L/min, these techniques allow FiO2 of 30% to 60%
Oxygen cages are closed environments where higher FiO2 can be achieved (>60%).
Nasal cannula: F
IVFT
endpoints of SpO2 >94% (or PaO2 >80) and [Hb] >8 (or hematocrit >24%)
acidemic and would benefit from a buffered isotonic crystalloid
for hypovolemia, an isotonic crystalloid should be administered at a shock
rate (dogs, 20 mL/kg, up to 90 mL/kg; cats, 10 mL/kg, up to 40–50 mL/kg) over 15 minutes, and then EOR should be reassessed
Volumes of colloids exceeding 22 mL/kg/day may impair coagulation, interfering with von Willebrand factor and factor VIII activity
Hypertonic saline (NaCl 7.0% to 7.5%, administered at 2 to 6 mL/kg, and typically no faster than 1 mL/kg/min
whole blood (20 to 25 mL/kg), packed red blood cells (10 to 15 mL/kg), or hemoglobin-based oxygen carriers (Oxyglobin)
hypotensive resuscitation for patients with active hemorrhage
vasopressors or inotropes
dopamine: 2-3mcg/kg/min, b=adrenergc activity, Causes vasodilation through activation of dopaminergic receptor
noradrenalin: 0.1-2, Primarily α agonist
Phenylephrine 1-3, potent vasoconstrictor
other Tx
o Early enteral feeding, if feasible, is preferred because it supports gastrointestinal integrity, thus minimizing bacterial translocation
analgesia and/or sedation
cardiogenic shock is oxygen supplementation
Distributive Shock and Sepsis
SIRS – systemic inflammatory response to infectious or noninfectious
marked decrease in systemic vascular resistance caused by loss of vascular tone and massive vasodilation.
by anaphylaxis (anaphylactic shock), severe damage to the central nervous system (neurogenic shock), or drugs, but most frequently is associated with systemic inflammatory response syndrome (SIRS) and sepsis.
pathophysiology
Different bacterial products (e.g., lipopolysaccharide, a component of the bacterial cell wall) = potent activators of the host response
bind on specific macrophage receptors
induce the production of proinflammatory mediators and cytokines
accumulation of inflammatory cells in capillary beds and peripheral tissues
> Microthrombi, endothelial cell swelling, and leukocyte accumulation
major organ systems are damaged by hypoperfusion, cytopathic hypoxia, ischemia-reperfusion injuries (ARDS)
Sepsis impairs the function of the cardiovascular system, affecting the myocardium, vessels, and coagulation, and thus contributing to acute circulatory failure
CS
compensated phase (hyperdynamic or warm) or a decompensated phase (hypodynamic or cold)
Cats with sepsis often present with hypothermia, bradycardia, normal to pale or icteric mucous membranes, and nonspecific pain
treatment
restore perfusion, identification and eradication of septic foci, and supportive care to prevent organ dysfunction
o Early Goal-Directed Therapy
MAP >65 mm Hg, urine output >0.5 mL/kg, and CVP 8 to 12 mm Hg
four-quadrant” therapy effective against Gram-positive and Gram-negative aerobes and anaerobes
Low-dose (physiologic) glucocorticoid in vasopressor-refractory hypotension
o Glucose Control
Clindamycin and enrofloxacin
Retrospective evaluation of the
indications, safety and effects of
fresh frozen plasma transfusions
in 36 cats (2014–2018)
Mansi 2020 JFMS
Thirty-six cats received 54 FFP transfusions
Eighteen of these cats had improved coagulation times after receiving 1–3 units
15% transfusion reaction
