week 3 shock Flashcards
oxygenation
diffusion of oxygen from lungs into blood
Ventilation:
gas exchange in the respiratory system (i.e., mechanics of air moving in and out of the lungs)
2 types of ventilation:
Pulmonary ventilation: total exchange of gases between atmosphere & lungs
Alveolar ventilation: exchange of gases within gas exchange portion of lung
Perfusion:
-adequate blood circulation through pulmonary blood vessels
-If blood supply inadequate, oxygenation is inadequate
-Perfusion is generated & maintained by three functions:
Pumping action of heart
Blood vessels
Blood volume
cellular effect of shock
-Impaired cellular metabolism causes:
Release of vasoactive inflammatory mediators, including histamine
Increased production of oxygen free radicals
Excessive lactic acid & hydrogen ions causing intracellular acidity
-promoting cellular dysfunction and death
shock
-Shock: derangement of oxygen delivery & consumption at a cellular level.
why body changes to anaerobic
Anaerobic- body has lack of blood (not being pumped fast enough or loss of blood) therefore lack of oxygen- so must convert to anaerobic-
what happens in anaerobic metabolism
- glycolysis is to slow to make enough ATP that body needs
- so Pyruvate is converted into lactic acid which heart can use as fuel.
- however this accumulates in cell & diffuses into extracellular fluid, damaging internal and external portions of cell as to acidic (E.g. lactic acidosis in shock)
conversion out of anaerobic
Conversion of pyruvate to lactic acid is reversible if oxygen supply is restored
Lactic acid converted back to pyruvate, & used for energy or to synthesis glucose
WHY DO WE CARE ABOUT ATP PRODUCTION
because lactic acid impairs Sodium-Potassium pump operation
-this results in excess sodium in cells- causes cellular oedema & increased cell membrane permeability
-Results in cellular death & release of intracellular contents to extracellular space causing further damage
-Lactic acid accumulates in intracellular & extracellular spaces
Causes further damage
Sympathetic response
Extrinsic reflexes and Higher neural control centre (chemo and baro receptors) activate sympathetic response.
-epinephrine & norepinephrine released, AND activation of alpha & beta (adrenergic) receptors
-Alpha receptors: vasoconstriction
Constriction of small arterioles & arteries, increased peripheral vascular resistance
-Beta 1 receptors: increase in heart rate and force of contraction
-B2 receptors: vasodilatation of skeletal muscle & relaxation of bronchioles
Increasing HR & systemic vasoconstriction, as well as dilation of bronchioles in the lung – fight or flight!
REnin angiotensin aldosterone system
Kidneys: major role in regulating arterial BP & altering blood volume
Kidney perfusion decreases when arterial BP drops
In response, kidneys produce & release renin from juxtaglomerular apparatus (JGA)
Renin catalyses reactions producing Angiotensin 2 (in blood)
Angiotensin II acts on blood vessels, causing vasoconstriction
Also acts on adrenal gland, causing aldosterone release
Causes kidney tubules to increase sodium reabsorption, resulting in more fluid being retained (water follows salt; thus, vascular blood volume & arterial blood pressure increased)
Contributes to long-term BP regulation
hypovalemic shock
- Diminished blood volume resulting in inadequate vascular filling – i.e. no blood/fluid in the circulatory system
- Most common form of shock
- May also cause third-space losses, where extracellular fluid shifts from the vascular compartment to interstitial space (surrounding tissues)
- Occurs with acute loss of 15-20% of circulating volume (70kg adult 850mls
- Acute, fatal haemorrhagic shock categorised by metabolic acidosis, hypothermia & coagulopathy
hypovaleic shock compesatory mechanisms
Compensation- your bodies little (periphreal) vessels tighten up to try and keep up O2 levels
hypovalemic shock-The “Deadly” Trauma Triad:
as core temperature decreases, so does body’s ability to stop bleeding as cold temp increasing blood viscosity. which the body then tries to correct by vasodilating- causing more bleeding
coagulopathy-(lactic acidosis)-acidosis(decreased myocardial efficiency)-hypothermia(inhibiting coagulation cascade)
cardiogenic shock
- Heart pumps blood insufficiently to meet body’s demands
- Stroke volume & cardiac output is reduced
- Coronary artery perfusion eventually impaired due to increased preload and afterload so no oxygenation occurs around body
- observed with-Decreased cardiac output, Hypotension, Hypo-perfusion, Indications of tissue hypoxia
intrinsic and exstrinsic effects of cardiogenic shock
intrinsic-MI (most common cause of cardiogenic shock), Arrhythmia, Valve defect, Ventricular aneurysm
extrinsic-Pulmonary embolism
Tension pneumothorax
Cardiac tamponade
obstructive shock
Due to mechanical obstruction of blood flow through central circulation (great veins, heart or lungs)
Causes increased right heart pressure due to impaired function (blood backlogging)
Pressures continue to increase, despite impaired venous return to heart
causes-Pulmonary embolism (common cause – lodges in part of lungs, impairing normal perfusion & increasing pressure of RV)
Dissecting aortic aneurysm
Pneumothorax
Haemothorax
Atrial myxoma (tumor)
Abdominal evisceration into thoracic cavity (ruptured hemidiaphragm)
distributive shock
Although blood volume has not changed for some reason vasculature expands until normal blood volume doesn’t fill circulatory system
Blood volume is redistributed, because circulatory vasculature expands, blood is randomly placed around body.
2 main causes-Decreased sympathetic control,
Excessive vasodilatory substances released
-includes neurogenic, anaphalaxtic shock, septic shock
neurogenic shock
Neurogenic shock is also known as spinal shock -common-among patients with a spinal cord injury above the mid-thoracic region, due to interruption of the outflow transmission from the vasomotor centre. Spinal shock may or may not be transient.
septic shock
- May occur as a result of bacterial, fungal, viral or parasitic infection (bacterial most common)
- Infection: pathogen invades body & overcomes host defences
- Pathogen colonises, binding toll-like receptors (TLRs) on surface of immune cells (monocytes)
- Initiates innate immune response to control infection with release of pro-inflammatory cytokines
- Pro-inflammatory response (causes Oedema to occur around infection site; variety of organisms contained within fluid- which stop infection)
- This promotes healing by limiting movement of infection, providing essential nutrients, & attracting immune cells
when infection reaches blood-septic shock
If infection enters bloodstream, affecting locations distant to site of origin, pro-inflammatory processes may be amplified
May cause profound & systemic state of inflammation
(this only alows infection to travel around body faster)
what body does to try and inhibit infection
-Macrophages release cytokines
- these exaggerate vasodilation, increasing cellular permeability to assist transportation of pro-inflammatory mediators to site
-Complement pathway also initiated
IL-1β & IL-6 stimulate hypothalamus to increase body temperature, accelerating tissue repair & inhibiting bacterial reproduction
sepsis
when immune system can not clear infection and it moves to the blood. Occurs with imbalance in regulatory mechanisms between pro- & anti-inflammatory mediators
Anti-inflammatory cytokines include IL-4, IL-10, IL-11, IL-13
Excessive pro-inflammatory response & failure of anti-inflammatory mediators to provide negative feedback
CONCEQUENCES OF SEPSIS
Causes altered coagulation, endothelial cell damage, widespread vasodilation, increased capillary permeability, & abnormal blood flow, reduced perfusion of vital organs
THIS LEADS TO….
-Hypovalemia due to peripheral pooling of blood & fluid loss into interstitial space
-organ dysfunction due to hypo-perfusion
as abnormal blood flow results in endothelial cell disruption, causing capillary leakage and impaired gas exchange.
-VO2 is increased without raised tissue metabolic activity, resulting in mitochondrial dysfunction
-Lactic acidosis occurs with switch to anaerobic metabolism
