shock and sepsis in the surgical patient Flashcards
shock
decline in vital organ function as a result of maldistribution of blood flow such that delivery of oxygen and nutrients to tissues is inadequate
state of inadequate tissue oxygenation
main causes of shock
hypovolemic
distributive
cardiogenic
hypovolemic shock
hemorrhage due to trauma, neoplasia, coagulopathy, RBC destruction, surgergy
classification of hypovolemic shock
mild: 10 to 15% blood loss
moderate: 30 to 35% blood loss, systolic BP 70 to 80
severe: 35 to 40% blood loss, systolic BP 50 to 70
profound: 40 to 50% blood loss, systolic BP <50
causes of hypovolemic shock
severe vomiting/diarrhea
hemorrhagic gastroenteritis
pancreatitis
burns
ascites
peritonitis
both diabetes
adrenocortical insufficiency
cardiogenic shock
failure of pump function of heart
myopathic, intracardiac or pericardial causes
reasons for myopathic cardiogenic shock
cardiomyopathy
myocardial infarction
myocardial contusion
myocarditis
reasons for intracardiac cardiogenic shock
ruptured chordae tendineae
acute aortic regurgitation
aortic stenosis
hypertrophy
arrhythmias
reasons for pericardial cardiogenic shock
neoplasia
idiopathic
coagulopathy
trauma
intraoperative cardiogenic shock flow chart
distributive shock causes
traumatic
anaphylactic
septic
how does trauma cause distributiv shock?
tissue damage leads to inflammatory response
tissue factors, endothelins, epinephrine
how does anaphylasis causes distributive shock?
histamine
bradykinin
serotonin
how does sepsis cause distributive shock?
bacterial toxins cause the release nitric oxide, tumor necrosis factor, eiconasoids
initial response of body to those 3 kinds of shock
what is the shock organ of a dog? What happens?
GI tract
shunt blood away from mesentery
decreased GI integrity
ulceration
melena
ileus
danger of bacterial translocation
what is the shock organ in a cat? what happens?
the lung
pulmonary edema
pleural effusion
acute respiratory distress syndrome
respiratory failure
stages of shock
compensatory
early decompensatory
late decompensatory
compensatory stage of shock
decreased venous return
decreased cardiac output
release of catecholamines
release of aldosterone, ADH
activation of renin-angiotension system
all of the above leads to increased HR, contractility and cardiac output
clinical signs of compensatory stage
tachycardic
tachypnic
BP may be normal
hyperdynamic stage
varies in length dependinng on insult
may not be seen clinically
early decompensatory stage
significantly decreased cardiac output
increased! sympathetic response
shunting of blood to brain and heart
all the above lead to:
decreased oxygen delivery
anaerobic glycolysis
cellular swelling
cell death
clinical signs of early decompensatory stage
tachycardia (or bradycardia in cats)
hypothermia
pale MM
prolonged CRT
cold limbs and skin
muscle weakness
decreased level of consciousness
oliguria
why do cats become bradycardic during the early compensatory stage of shock?
increased parasympathetic response
increased myocardial depressant factor
late decompensatory stage
prolonged tissue hypoxia
circulatory collapse
insufficienct cerebral and cardiac blood flow
leads to organ failure and cardiopulmonary arrest
clinical signs of late decompensatory stage
refractory hypotension
absent pulses
damaged myocardium causes decreased cardiac output
pale or cyanotic MM
absert CRT
severe hypothermia
anuric renal failure
pulmonary edema
petechia, hemorrhage
GI sloughing
goals for therapy for shock
restore tissue perfusion and oxygen delivery
ensure adequate respiration
control hemorrhage
expand circulating blood volume
ABCs
ABCs of therapy for shock
Airway: patent airway, oxygen
Breathing: diuretics, bronchodilators, thoracocentesis, chest tube, intubation, ventilation, pain management
circulation: IV crystalloids, colloids, blood products, vasopressor agents, anti-arrhythmics
fluid support for shock
Crystalloids: isotonics, hypertonic, hypotonic
colloids: hetastarch, pentastarch, vetstarch, human/canine albumin
blood products: Packed RBCs, fresh frozen plasma, fresh whole blood
sepsis
systemic response to infection with bacteria, viral or protozoal organisms
septic shock
sepsis with hypotension despite adequate fluid resuscitation
pathophysiology of sepsis
LPS and peptidoglycans stimulate inflammatory target cells (mononuclear cells, PMN, vascular endothelial cells, plts
what happens in sepsis after mediators are released?
vasodilationo
increased vascular permeability
initiation of complement cascade
further recruitment of neutrophils and macrophages
activation of coagulation
consequences of vasodilation in sepsis
hypotension
decreased organ and tissue perfusion
ischemia-organ damage
venodilation: decreased preload
myocardial depression
consequences of activating coagulation during sepsis
Disseminated intravascular coagulation-thrombocytopenia, hypofibrinogenemia, elevates FSP, PT, PTT and D-dimers
bleeding tendencies
microthrombosis of small vessels
organs ischemia and hypoperfusion
clinical signs of sepsis
dereased mentation
weak
collapsing
abdominal pain
dyspnea/tachypnea
tachycardia
fever/hypothermmia
poor pulses
injected mucous membranes
diagnosis of sepsis
good PE
mentation, hydration, perfusion indices
heart murmur, arrhythmia
respiratory effort, lung sounds
abdominal palpation-pain, mass, fluid wave, foreign body, intestinal sounds
evidence of skin lesions
swollen/painful/warm joints
diagnostics of sepsis
CBC, Chem23, UA
coagulation profile, blood gas analysis
cultures!
rads, u/s
abdominocentesis, thoracocentesis, arthrocentesis
fluid analysis
treatment of sepsis
surgical correction
fluid balance
BP
treat underlying disease
treat DIC: fresh frozen plasma, +/- heparin
oxygen therapy
pain meds
nutrition
monitor!
prognosis of sepsis
depends on underlying disease process and status of cardiovascular system
mortality rate 25-60%
