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Shock at the cellular level

diffusion of oxygen from lungs into blood oxygenation
760mHg atmospheric pressure at sea level
total exchange of gases between atmosphere and lungs pulmonary ventilation
exchange of gases in the alveoli alveolar ventilation
derangement of oxygen delivery and consumption at a cellular level shock
stronger faster heartbeat, vessel dilation, vessel constriction to nonessential organs sympathetic response
located in carotid arteries and aortic arch, respond to changes in stretch of the vessel walls baroreceptors
monitor O2, CO2 &H+ in carotid bodies chemoreceptors
responses associated with pain/cold factors extrinsic reflexes
detects vasoconstriction alpha receptors
detects increase in heart rate and force of contraction beta 1 receptors
vasodilation of skeletal muscle and relaxation of bronchioles beta 2 receptors
neural response: hypothalamus releases corticotropin
neural response: corticotropin stimulates pituatary gland to release adrenocorticotropin hormone
ACTH stimulates adrenal gland to release cortisol (hyperglycaemic hormone)
elevates blood sugar level and stimulate Na and water retention hyperglycaemic hormone
when kidney perfusion decreases arterial bp drops
in response to bp drop, kidneys release what from the juxtaglomerular apparatus? renin
renin does what to produce angiotensin II catalyses the reaction
angiotensin II acts on blood vessels causing vasoconstriction
angiotensin II acts on which gland to cause aldosterone release adrenal gland
causes kidney tubules to increase sodium reabsorption, which causes water retention angiotensin II
causes vascular blood volume and arterial bp to increase water retension
in response to bp drop, osmoreceptors in the hypothalamus stiumulate what to release ADH posterior pituatary gland
decrease in blood volume, pressure and increase in osmolality of bodily fluids is triggers what? osmoreceptors
directly vasoconstricts and causes water reabsorption anti-diuretic hormone
when only glycolysis is functioning to produce ATP, respiration is said to be anaerobic
when both glycolysis and the krebs cycle are functioning to produce ATP, respiration is said to be aerobic
in anaerobic respiration, pyruvate converts to lactic acid
in aerobic respiration, pyruvate converts to 2 acetyl CoA
lactic acid accumulation impairs the Na+/K+ pump
impairment of the Na+/K+ pump results in excess intracellular Na+
excess intracellular sodium causes cellular oedema and increased membrane permeability
cellular oedema results in cell lysing
anaerobic cell lysing results in lactic acid in the extracellular space
impaired cellular metabolism releases vasoactive inflammatory mediators
impaired cellular metabolism increases production of oxygen free radicals
impaired cellular metabolism results in excessive lactic acid and H+ ions
diminished blood volume resulting in inadequate vascular filling hypovolaemic shock
how much blood loss for hypovolaemic shock 15-20%
how much blood volume per kilo of a human being 70ml
heart pumps blood insufficiently to meet body's demands cardiogenic shock
increase LV end systolic volume increase in preload
increase in end systolic volume and preload when paired with decreased myocardial contractility increase in afterload
coronary artery impairment both increase in preload and afterload
Decreased CO, HOTN, hypoperfusion, tissue hypoxia despite adequate intravascular volume. cardiogenic shock definition
MI, arrhythmia, valve defect, ventricular aneurysm intrinsic factors of cardiogenic shock
Pulmonary embolism, tension pneumothorax, cardiac tamponade extrinsic factors of cardiogenic shock
due to mechanical obstruction of blood flow through central circulation obstructive shock
PE, dissecting aortic aneurysm, pneumothorax, hameothorax, atrial myxoma, hemidiaphragm factors of obstructive shock
myocardium contracts against high afterload p1 obstructive shock
sympathetic activation causes vasoconstriction to maintain bp p2 obstructive shock
normal BP maintained but organ perfusion decreased p3 obstructive shock
increased pressure causes venous congestion p4 obstructive shock
vasculature expands until normal blood volume doesnt fill circulatory system distributive shock
loss of vessel tone, enlarged vascular compartment, displaced vascular vol from central circulation signs of distributive shock
decreased sympathetic control, excessivevasodilatory substances released causes of distributive shock
brain injury, CNS depressing drugs, general anaesthesia, hypoxia or lack of glucose causes of neurogenic shock
hypotension, warm skin due to loss of cutaneous control symptoms of neurogenic shock
loss of sympathetic control above T6 causing loss of vasomotor tone neurogenic shock
an inflammatory response initiated by presence of organism in normally sterile tissue infection
presence of live bacteria in bloodstream bacteraemia
presence of pathogen in bloodstream leading to sepsis septicaemia
syndrome comprising of set clinical signs in response to systemic inflammation Systemic inflammatory response syndrome
orignially defined as SIRS triggered by a primary localised infection Sepsis
bacterial, fungal, viral or parasitic infection causes of sepsis
pathogen invasion p1 sepsis
pathogen binds to toll-like receptors on monocytes p2 sepsis
release of pro inflammatory cytokines to control infection p3 sepsis
macrophages release TNF-A, IL-B1, IL-2, IL-6 increases NO release from endothelial cells, vasodilation, and cellular permeability, and initiated compliment pathway`
stimulate hypothalamus to incrs temp IL-1 and IL-6
IL-4, IL-10, IL-1, IL-13 anti-inflammatory cytokines
failure to balance pro and anti-inflammatory mechanisms altered coagulation, endothelial cell damage, vasodilation, increased capillary permeability and abnormal blood flow (perfusion).
can develop with hypoperfusion and hypoxia widespread, resulting in lactic acid build up and change of metabolism Multiple organ dysfunction syndrome
activated endothelial cells release pro-thrombotic factors to compensate for blood loss (factor VII), but then attempts to break down the clots, causing widespread bleeding,tissue ischaema. disseminated intravascular coagulation
multiple small thrombi/emboli form in small blood vessels resulting in occlusion thrombotic phase
fribrinolysis of thrombi occurs, suppressing thrombin and further aggravating bleeding fibrinolytic phase
life threatening organ dysfunction caused by disregulated host response to infection septic shock
RR>22/min, change in GCS, systolic blood pressure </= 100mmHg Quick Sequential Organ failure Assessment
hypoperfusion causes alveolar and capillary wall damage, incrs surfactant, leaky tissues, gas exchange impaired, decreased organ/tissue perfusion, and organ failure Acute Respiratory Distress Syndrome
Sudden interruption of renal function, decreased glomerular filtration rate, and reabsorption of Na and H2O resulting in renal necrosis Acute Renal Failure
Created by: 1092422624234171



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