Shock Flashcards
List types of shock
circulatory shock:
- hypovolemia
- maldistributive
- cardiogenic
- obstructive
anemia
hypoxemia
impaired cellular oxygen utilization and energy production
What is the broad definition of shock?
the VO2 exceeds DO2 and utilization –> leading to a cellular energy debt and measurable organ dysfunction
other more common now: impaired cellular energy production
DO2 is a function of ____ and ____
DO2 is a function of CO and CaO2
CaO2 = ___ x ___ x ___ + ___
CaO2 = 1.34 x Hb x SO2 + 0.003 PaO2
Fill in the blanks
Explain how the delivery-independent Oxygen cosumption can be maintaned
- DO2 in excess of VO2
- Oxygen extraction only 25% under normal circumstances. Can be increased to 70-80% if DO2 is decreased
When does oxygen consumption become delivery dependent?
When the DO2 drops to a point when oxygen extraction cannot be increased enough to compensate and VO2 will drop with further decline in DO2
what are the intracellular consequences of decreased O2 delivery and consumption?
decreased DO2 and VO2 –> decreased oxidative phosphorylation/electron transport chain in the mitochondria to produce ATP
–> cells respond by reducing metabolic activity
eventually switch to anaerobic metabolism –> lactate production
–> intracellular acidosis: denaturation of proteins, decreased enzyme function, disruption of transport mechanisms
inadequate cellular energy –> intracellular systems fail (ion pumps fail, oxygen free radical formation, loss of adenine nucleotides) –> tissue injury
ion pumps fail –> membrane integrity of cells fail –> fluid shifts into cells –> cellular edema
–> cellular necrosis or triggering of apoptosis
What are the 3 stages of shock?
- compensated shock
- decompensated shock
- terminal/irreversible shock
Explain the pathophysiology of compensated shock
the body is attempting to maintain core tissue/organ perfusion
- baroreceptors sense decreased vessel wall tension
- chemoreceptors sense hypoxia/hypercapnia/acidemia
► cathecholamine release
► tachycardia, increased cardiac contracility, peripheral vasoconstriction
► restores mean arterial perfusion pressure ► preserves perfusion of core organs
also: activation of RAAS system and increased release of vasopressin ► additional vasoconstriction + decreased urinary water loss
also: decrease in hydrostatic pressure (if applicable) ► water movement from itnerstitial into intravascular compartment
May happen at the expense of peripheral and splanchnic circulation ► hypoxic damage happens here already in compensated phase of shock
Explain the pathophysiology of decompensated shock
compensatory mechanisms are overwhelmed/exhausted
► impaired core perfusion
- hypotension ► hypoperfusion ► hyperlactatemia ► metabolic (lactic) acidosis ► progressive catecholamine insensitivty
► vasodilation/ loss of vasomotor tone ► impaired venous return ► decrease in CO
► bradycardia ► decrease in CO
► irreversible/terminal shock
List 5 groups of complications arising from shock
- Systemic inflammatory response
- Coagulopathy
- Mitochondrial dysfunction
- Microcirculatory dysfunction
- Multiple organ dysfunction syndrome
What are the causes for systemic inflammation in shock?
- upregulation and release of inflammatory cytokines, e.g., IL-6, G-CSF
- IL-6 and G-CSF serve as chemotactic factors ► neutrophil infiltration into affected tissues ► diapedesis
- ► neutrophils release reactive oxygen and nitrogen species and proteolytic enzymes
- ► vasodilation, increased capillary permeability, dectruction of extracellular matrix
- ► tissue edema ► decreased O2 and metabolite exchange ► cellular dysfunction
- neutrophil plugging on endothelium ► vessel obstruction ► disruption of microcirculatory blood flow
- activation of the complement system
- tissue injury ► release of split products, e.g., C3a, C5a (i.e., anaphylactoxins)
- lead to
- ► increased vascular permeability
- ► histamine and arachidonic acid product release
- ► cytokine production and release,
- ► promote aggregation and adherence of granulocytes to endothelium
increased activity of phospholipases A2 and C
- stimulates production of prostaglandins and leukotrienes
- ► further recruitment of inflamamtory cells
- ► alterations in vascular permeability
- ► impaired vasomotor tone
- ► enhanced platelet activity and aggregation
“shock gut”
- decreased intestinal perfusion ► increased intestinal permeability ► bacterial translocation
after reperfusion ► release of toxic metabolites and reactive oxygen species
- hypoxanthines accumulate during ischemia
- reperfusion ► O2 reintroduced ► formation of ROS
- lipid peroxidation, membrane disruption, DNA damage
- ► further cell damage ► necrosis and apoptosis
Explain how shock leads to coagulopathy
shock ► systemic inflammation
- inflammatory cytokines (IL-1, IL-6, TNF-alpha, arachidonic acid metabolites) ► procoagulant
- increased expression of tissue factor on endothelium and monocytes
- consumption and downregulation of natural anticoagulants (protein C, antithrombin
- increased activity of Plasminogen-activator-inhibitor (PAI-1) and thrombin-activatable fibrinolysis inhibitor (TAFI)
► hypercoagulable state ► microthrombi
- arterial clots ► impairs tissue perfusion
- venous clots ► impairs venous return and oxygenation (if PTE)
►consumption of clotting factors + platelets ► hypocoagulable state
Explain how shock causes mitochondrial damage
- inflammatory cytokines (e.g., TNF-alpha) ► uncoupling of oxidative phosphorylation, increased mitochondrial permeability and apoptosis
- increased production of reactive oxygen and nitrogen species and decreased ability to scavange free radicals
- reperfusion injury (increased free radicals)
During shock, what leads to microvascular derangements, other than decreased perfusion?
- endothelial edema from ischemic injury ► increaed wall thickness decreases diameter
- increased permeability
- damage from inflammatory mediators ► inflammation ► endothelial activation ► leukocyte adhesion and capillary plugging
- arterial microthrombi ► impaired blood flow
Explain how the gastrointestinal tract is compromised during shock
►splanchnic and peripheral circulation is first to be compromised during compensatory vasoconstriction to preserve perfusion of vital organs ► ischemic injury
►epithelial injury and loss of mucosal barrier ► bacterial translocation
► reperfusion injury ► shown to cause dysmotility
Briefly describe the pathophysiology of ARDS
- ARDS involves inflammation-induced diffuse alveolar-capillary injury and subsequent severe accumulation of proteinaceous edema in the pulmonary interstitium and alveoli
List 3 examples of DAMPs released during cell death from shock
mitochondrial DNA
histones
heat shock proteins
List 8 compensatory mechanisms being initiated during shock
- baroreceptors (sense decreased stretch) - decreased inhibition of sympathetic tone - increases vasoconstriction, HR and contractility
- peripheral chemoreceptors (sense increased CO2, decreased pH and O2) - vasoconstriction and increasing HR
- central chemoreceptors (medulla oblongate, senses pH/CO2) - increased RR and TV
- decreased capillary hydrostatic pressure causes reabsorption of volume from interstitium
- increased circulating catecholamines and endorphine - vasoconstriction and decreases pain perception
- hyperglycemia - from upregulated hepatic gluconeogenesis
- RAAS upregulation
- ADH synthesis and release - secondary to hypothalamus sensing decreased ECV
What causes neurogenic shock?
abnormally low sympathetic tone and unopposed parasympathetic stimulation of vascular smooth muscles
typically TBI or spinal cord injuries
causes distributive shock
What is a normal CVP in a well-perfused patient?
0-6 cm H2O
What can cause decreased SvO2
- decreased DO2 (
- increased VO2 (e.g., hyperthermia, fever, seizures)
What can cause an increased SvO2?
hyperdynamic stage of sepsis
cytotoxic tissue hypoxia (e.g., cyanide toxicity)
Compare SvO2 and ScvO2 in critically ill patients with circulatory failure versus in health
health
* SvO2 > ScvO2 - higher oxygen extraction ratio of the brain, lowest OER of the kidneys
critically ill
* SvO2 < ScvO2 - blood preferentially diverted to brain and heart, splanchnic contraction - higher OER due to less perfusion
What part of the hypothalamus senses plasma osmolality?
supraoptic and paraventricular nuclei
Describe the ROSE principle
Resuscitation
Optimization
Stabilization
Evacuation
What is the Mark-Phillips curve?
Curve showing changes in extravascular lung water in response to increases in preload
can be used superimposed to the Frank-Starling’s curve, showing how fluid unresponsive patients have significant increases in lung water compared to preload increases
What is the Passive Leg Raise?
Leg raise in people - equivalent to a mini fluid bolus as it distributes fluids to the central circulation - patient can then be assessed for signs of fluid overload or fails to respond - this can be reversed
equivalent in dogs would be a mini bolus of 3-5 mL/kg
What is the equation for venous return?
Venous return = (MCFP - RAP) / venous resistance
What was the sensitivity of chest radiographs to detedct hypovolemia in traumatized cats?
only 19%
look for cardiac size, CVC and pulmonary vessel diameter
List the disadvantages of using CVP for intravascular volume assessment
- static parameter
- poor surrogate for RAP, cardiac filling pressure, or preload changes (ventricular pressure-volume curve is not linear)
- affected by cardiac, lung, and intrathoracic pressures
- invasive
- expensive
- technically demanding
- associated with complications
List 3 sites for caudal vena cava diameter measurements
- suprailiac (kidney)
- right intercostal (transhepatic)
- subxiphoid (diaphragmatic)
Which view for caudal vena cava diameter measurements has the lowest inter-rater variability?
subxiphoid view
Of the cardiac POCUS measurements, which is the most sensitive to detect volume status changes?
LA size (this is just the authors opinion, not referenced)
How does the Marik-Philips curve change in a septic patient?
towards the left
i.e., same preload causes more increase in extravascular lung water
Fluid responsiveness is indicated by a PPV or SPV of greater than XX to XXX %
greater than 10-15%
What are influences that could falsely alter the PPV or SPV?
- spontaneous breathing effort agaisnt vent
- altered chest wall compliance
- cardiac disorders like arrhythmias
- right heart failure
- altered intrabdominal pressure
How do you calculate PPV?
(P max - P min) / [(P max + Pmin)/2] x 100
How do you calculate the CVC collapsibility index?
CVCCI = (CVC d max - CVC d min) / CVC d max
What CVC collapsibility cutoffs describes fluid responsiveness?
> 50%
What is VTI AO?
volume time integral in the left ventricular outflow tract
can be used to calculate CO
List adverse effects from crystalloid fluid resuscitation (6)
- pulmonary edema and acute lung injury from fluid overload
- GI: decreased motility and increased permeability - risk of bacterial translocation and abdominal compartment syndrome
- Heart: ventricular arrhythmias, decreased contractility, decreased CO (if reaching past point of fluid responsiveness on the Starling’s curve)
- Coagulation: dilution of coag factors and decreased viscosity can cause coagulopathy
- Inflammation: D-lactate (LRS) can cause neutrophil stimulation; decreased osmolality»_space; cell swelling»_space; phospholipase A2 activation, TNFalpha and interleukin production
- Glycocalyx damage
List 3 definitions of massive transfusion
- patient blood volume or greater over 24 hours
- 50% patient blood volume over 3 hours
- 1.5 mL/kg/min over 20 min
What is the current evidence for synthetic colloid induced AKI in dogs and cats?
dogs:
* inconsistent results - some show increased risk of AKI proportionate to the dose and duration, others showed no difference
* marginal increase in biomarkers for tubular injury or renal inflammation
cats:
* 2 studies, neither found increased risk of AKI or mortality
No randomized controlled trials atm
Which clotting factors are mostly affected by synthetic colloid induced coagulopathies?
FVIII
vWF
Besides increasing intravascular volume, what are benefits of hypertonic saline administration?
- immunomodulatory effects - decreases neutrophil activation/adherence, decreases lymphocyte proliferation, inhibits inflammatory cytokine production
- decreases intracranial pressure
- reduces endothelial cell swelling
- improves myocardial function and causes coronary vasodilation
Why could PaCO2 potentially increase in a state of shock?
Increased H+ production»_space; intracellular buffering»_space; increased CO2 production
usually compensated for though by hyperventilation
How is RAAS activated during shock and what are its effects?
activated by:
* sympathetic innervation
* decreased afferent arteriolar stretch
* decreased Cl delivery to the macula densa
effects:
* peripheral vasoconstriction
* efferent arteriolar vasoconstriction»_space; maintains GFR
* increased NaCl absorption
* aldosterone release from adrenal cortex (zona glomerulosa)»_space; increased NaCl absorption
* ADH release triggered
Why do patients with decompensated shock develop bradycardia and decreased contractility?
- progressive intracellular acidosis»_space; reduces IC Ca++ cc»_space; decreased contractility
- intracellular acidosis»_space; impairs conduction system»_space; bradycardia
Waht could be used as a surrogate for arterial BP waveforms when trying to assess pulse pressure variations?
Pulse oximeter plethysmograph
In hypovolemic shock, what may change on the ECG?
R wave amplitude decreases
What does Pv-aCO2 indicate?
increased values indicate tissue CO2 production
indicator for cardiac output
What can you assess by dividing Cv-aCO2 by Ca-vO2?
indicator of anaerobic metabolism by tissues
Why is LRS theoretically a better choice than Norm-R/Plasmalyte to treat hypovolemic shock?
acetate may cause vasodilation
What is the definition of Cardiogenic shock and how is it clinical diagnosed?
decreased cardiac output and tissue hypoxia despite adequate intravascular volume
hypotension (SAP<90, MAP<65) with severely decreased CI and elevated end-diastolic LV pressure (>18 mm Hg)
How does glucagon help in cardiogenic shock?
Has positive inotropic effects
adjunctive tx option for patients that are unresponsive to other inotropic gent
How do you calculate the oxygen extraction ratio?
OER (%) = (CaO2 - CvO2) / CaO2
CvO2 = mixed venous O2
calculate CvO2 with same formula as CaO2 formula but need mixed venous O2 saturation
In metanalyses, was lactate clearance or SvO2 correction as treatment guidance better at improvig survival?
lactate clearance-driven algorithms
Describe Near-Infrared Spectroscopy
- measures light absorption according to the Beer-Lambert law
- can measure tissue oxygen saturation (StO2)
- assuming status SaO2 - drop if StO2 indicated reduced perfusion
- can detect perfusion derangements before oximetry, palsma lactate, or physical exam can
- associated with disease severity but not survival in dogs
List 3 methods of microvascular visualization
- orthogonal polarized spectroscopy imaging
- sidestream dark field imaging
- Incident Darl Field imaging
How does transcutaenous O2 and CO2 monitoring work and what is its utility in critically ill dogs?
- approximately O2 and CO2 tension in tissues
- measures gas tension via polarography
- heats skin to 43-45 degrees C»_space; increases transcutaenous gas diffusion
in critically ill dogs»_space; overestimates PaO2 and PaCO2»_space; don’t use in these patients
What is regional capnography?
tonometer measuring PCO2 in tissues
» used to establish tissue-to-arterial PCO2 gradient
By what percentage can splenic contraction increase the RBC mass?
up to 20 %
At what percentage blood loss is irreversible shock and death imminent?
above 40-50%
What defines massive hemorrhage?
blood loss of total blood volume within 24 hours
or half blood volume within 3 hours
How effective are transcapillary fluid shifts at restoring blood volume?
up to 50% of plasma volume can return
What is Claudin-3?
intestinal tight junction protein - lost after hemorrhagic shock - needed to maintain the mucosal barrier
