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