shock Flashcards
what is shock?
systemic hypoperfusion or ograns
- hypoxia
- acidosis
- build up of toxins
what happens to kidneys during shock
tubular necrosis (acute)
- drop in renal function
- reduced production of urine (anuria)
components of ogran dysfunction
- cell and tissue hypoxia
- cytokines and secondary mediators diminish myocardial contractility and cardiac output (sepsis)
- decrease renal perfusion
- acute respiratory distress syndrome (from inflammatory mediators)
- brain hypoxia
- adrenal dysfunction (W-F syndrome)
metabolic abnormalities
- insulin resistance and hyperglycemia
2. lactic acidosis
insulin resistance with shock
- TNF, IL-1, stress induced hormones (glucagon, glucocorticoids)
- gluconeogenesis
- impaired surface expression of GLUT-4 glucose transporter
- initial surge of glucocorticoids followed by adrenal insufficiency and functional glucocorticoids deficits
key clinical feature of metabolic abnormalities
hyperglycemia
-poisons neutrophils
hypoperfusion=hypotension
BP= CO x PR
- CO: heart failure (cardiogenic), hypovolemic
- PR: inflammatory, anaphylactic
- COxPR: neurogenic (spinal), interferes with sympathetic, decreases peripheral resistance and bradycardia
cardiogenic and hypovolemia
skin turns pale, clammy and cold
-inadequate perfusion with increased peripheral resistance
systemic inflammatory and anaphylactic
inadequate pressure due to to decreased peripheral resistance
-skin is red and hot
neurogenic
decreased vascular resistance and bradycardia
cardiogenic symptoms from shock
ventricular fibrillation
heart failure
cardiac tamponade
saddle pulmonary embolus
hypovolemic symptoms of shock
hemorrhage-> intrinsic or extrinsic
dehydration
burns
stage 1 of hypovolemic shock
<15% volume loss (750mL) blood pressure: normal heart rate: normal appearance: pallor mental status: normal to anxious renal output: normal
stage 2 of hypovolemic shock
volume loss: 15-30% (750-1500ml) BP: systolic normal, diastolic high, narrow pulse pressure HR: >100bpm Appearance: pale, cold, clammy skin mental status: mildly anxious, restless renal output: 20-30 ml/hr
stage 3 of hypovolemic shock
volume loss: 30-40% (1500-2000ml)
BP: systolic 120bpm (increased RR as well, hyperventilating)
appearance: sweating, with cool, pale skin
mental status: confusion, anxiety, agitation
renal output: 20ml/hr
stage 4 of hypovolemic shock
volume loss: >40% (>2000ml)
BP: systolic 140 bpm (also hyperventilating)
appearance: skin is sweaty, cold, and extremely pale
mental status: decreased consciousness, lethargy, coma
renal output: negligible
most common cause of shock
staph. Aureus (G+)
sepsis implies
overwhelming systemic inflammation from bacteremia
- staph A. (toxic shock), E. coli most common
- also Klebsiella, streptococci, pseudomonas
in sepsis, what is the inflammatory response from?
production and distribution of inflammatory mediators
-“cytokine storm”
septic shock
presence of microbial organism cause systemic activation of endothelial and inflammatory cells
innate response in septic shock
recognition of microbial factors
-endotoxin-> LPS
-toxic shock-> superantigen (polyclonal T cell activation)
Complement activation
TLR
activation of coagulation factors (hageman factor)
release of inflammatory mediators
inflammatory and counter-inflammatory responses in septic shock
- TLR’s, PAMP’s, G-protein couple receptors, NOD1, NOD2
- TNF, IL-1, IL-6, IFN-gamma, IL-12, IL-18
- ROS, lipid mediators (PG, LT)
- complement cascade
endothelial cell activation and injury in septic shock
vasodilation, increased vascular permeability, coagulation
counter-regulatory immunosuppressive mechanisms in septic shock
shift from Th1 to Th2
anti-inflammatory mediators (soluble receptor blockers)
apoptosis of lymphocytes
hyperglycemia deactivation of neutrophils
anaphylactic shock
systemic release of histamine
vasodilation with increased vascular permeability-> secondary hypovolemic edema, ARDS
epinephrine-> increases vasoconstriction
systemic release of histamine in anaphylactic shock
anaphylaxis-> IgE mediated
anaphylactoid-> complement factors, radiocontrast material, anesthetic gasses
neurogenic shock
spinal shock
interruption of sympathetic impluses
DIC
- endothelial cell activation and injury
- vascular stasis in small vessels
- fibrin-rich thrombi in small vessels
- consumption of coagulation factors with disastrous results: fibrinolytic peptides, d-dimer
- waterhouse-friderichsen syndrome (bleeding into adrenal glands)
endothelial cell activation and injury in DIC
- production of pro-coagulant factors
- decreased endothelial anti-coagulant factors: TFI, thrombomodulin, protein C)
stages of shock
- non-progressive phase
- progressive stage
- irreverisble stage
non-progressive phase stage of shock
compensatory mechanism activated and perfusion is maintained
-neurohormonal response to shock
-activation of baroreceptors with catecholamine release
-activation of R-A
-ADH release
-generalized sympathetic stimulation
NET EFFECT: tachycardia, peripheral vasoconstriction, renal conservation of fluid
progressive stage of shock
tissue hypoxia with worsening circulatory and metabolic imbalances
- widespread tissue hypoxia
- intracellular aerobic respiration replaced by anaerobic glycolysis
- excessive production of lactic acid
- decreased tissue pH with dilation of arterioles
- peripheral pooling of blood
- anoxic injury to endothelium
- vital organs begin to fail
irreversible stage of shock
cellular and tissue injury is irreversible
- widespread injury
- lysoszomal enzyme leakage
- ischemic bowel with exposure to intestinal flora
- anuria, renal failure
morphology of septic shock
- widespread hypoxia cell and tissue injury
- adrenals-> cortical cell depletion (stress)
- kidneys-> acute tubular necrosis
- lungs-> resistance to hypoxic injury from hypovolemic shock, trauma or sepsis results in diffuse alveolar damage (chock lung)
- DIC with widespread deposition of fibrin-rich microthrombi: consumption of platelets and coagulation factors results in petechial hemorrhages on serosal surfaces and skin
