Circulatory shock
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- management of septic shock
- need to eliminate source of infection with the appropriate admin of antibiotics (penicillin= gram pos, chloramphenical= anaerobic, amphotericin= fungal
- causes of hypovolemic shock
- shift of internal fluid out of the intravascular compartments (internal hemorrhage or ascites) or external fluid shifts (fluid lost from the body), or diabetes insipidus or addison's (decr. aldosterone)
- cardiogenic shock
- inability of the heart to pump blood. decr CO results from impaired heart function (MI or valvular problems). primarily affects the L ventricle. b/c of the altered L ventricular function....causes decreased stroke vol and an incr LV pressure leads to incr pulmonary congestion.
- treatment for cardiogenic shock
- need to limit the amount of heart muscle damage ( early admin of thrombolytic agents, coronary angioplasty, and CABG). use measures to improve heart function (a positive inotropic agent...dobutamine, dopamine, amiodarone, and epinephrine). use vasodilators to improve pumping effectiveness of heart by reducing the preload and afterload (NTG, nitroprusside, phentolamine). the use of intra-aortic balloon pumping
- treatment for hypovolemic shock
- correct cause and increase intravascular volume with isotonic, hypotonic, or hypertonic solutions, blood products or plasma expanders
- circulatory shock
- a complex sydrome of decr blood flow to tissues resulting in eventual organ failure (MODS). when tissue perfusion is inadequate to supply oxygen and nutrients to body cells.
- isotonic fluid
- a crystalloid used to increase the intravascular volume. same tenacity as fluids in the intravascular space. will fill intravascular space s pulling fluids in or out of. 0.9NS, d5W, LR
- causes of cardiogenic shock
- caused by coronary problems (AMI or when there are problems with the LV wall) and noncoronary causative factors (valvular heart abnormalities, cardiac tamponade...fluid in the pericardium; or cardiomyopathies
- relative hypovolemia (third spacing)
- the result of fluid shifting from the vascular space into the extravascular space.
- treatment of septic shock
- need to provide supportive therapy. ventalation and oxygenation, increase intravascular volume, monitor RBC volume/O2 sat/CO/BP (may need vasopressors to maintain BP0. and metabolic balance....
- distributive or vasogenic shock
- an abnormality in the vascular system ( the plumbing) that produces a maldistribution of blood volume (includes neurogenic, anaphylactic, and septic shock). the heart is pumping adequately, volume is normal, and the intravascular volume is maldistributed
- management of neurogenic shock
- need to minimize spinal cord trauma by stabalizing the patient.
- HOrmonal compensation of shock
- SNS activation causes decr blood flow -> incr renin -> incr aldosterone -> incr Na and H2O retention. ant pit gland is stimulated to incr ACTH -> adrenal cortex incr cortisol production ->liver to incr blood glucose. and the adrenal medulla is stimulated to incr epineph/norephineph
- chemical compensation of shock
- SNS activation causes decr blood flow to lungs -> incr physiologic deadspace -> incr vent/perfusion imbalance -> decrarterial oxygen tension -> change in LOC and incr resp rate and depth ->incr exhalation of CO2 (hyoerventilation) ->decr arterial CO2 ->respiratory alkalosis
- neurogenic shock
- massive vasodilation d/t loss of elasticity and ability to constrict. the massive dilation causes peripheral pooling ->warm, moist skin -> less blood returns to cardiac (HPO)-> less oxygenated blood is recirculated. can occur within 30 min of a spinal cord injury of T5 or above.
- progressive stage
- the third stage of shock when the activated compensatory mechanisms cause multisystem dysfunction. clinical sx: low BP, high P, skin is cold/mottled/cyanotic, weak peripheral pulses, decr UOP ( less than 20 cc/hr...may lead to kidney damage down the road), decr LOC, shallow rapid resp, absent Bowel Sounds. lab data: incr AST, ALT, LDH (indicates liver dysfunction), CPK, BUN, and Cr (indicate kidney dysfunction); incr bleeding times (prolonged PT and PTT); decr pH, HCO3 (depending on acidosis or alkalosis), platelets, fibrinogen.
- absolute hypovolemia
- the result of fluid lost through hemorrhage, GI loss, fistula drainage, diabetes insipidus, hyperglycemi, or diuresis
- hypotonic fluid
- a crystalloid used to rehydrate cells. has a decreased tenacity than fluids in the intravascular space which helps to pull vol out of intravascular space to help rehydrate cells. 0.45NS (half NS)
- compensatory stage
- the second stage of shock when there is a decr CO and compensatory mechanisms are activated
- hypovolemic shock
- decreased intravascular volume. acute loss of 15-20% of circulating blood volume. compensatory mechanisms: vasoconstriction, fluid shift into vasculature, increased pumping efficiency of the heart
- septic shock
- a form of distributive shock that is associated c a severe overwhelming infection. sepsis most commonly caused by gram-negative organisms. the normal immune/antibody cascade responses are initiated and work together to destroy the antigen, but in sepsis the response to the antigen is exaggerated. increase in inflammation and coagulation and decr in fibrinolysis. endotoxins from the microorganism stimulate the release of cytokines and other proinflammatory mediators that act through secondary mediators such as platelet activating factors and interleukins. release of platelet activating factors results in the formation of microthrombi and obstruction of vasculature. total effects of mediators: damage to the endothelium, vasodilation, increased capillary permeability, and neutrophil and platelet aggregation and adhesion to the endothelium. Sx include fever, vasodilation, warm/flushed skin initiallym mild HTN, respiratory alkylosis initially, and inappropriate behavior. Pathophys includes host response meidated by complex hormonal and chemical substances, decr myocardial function and alterations in periph circulation (decr force of contraction and decr preload), periph alterations (massive vasodilation, maldistribution of blood vol, and incr capillary permeability)
- management of anaphylactic shock
- need to id and remove causative antigen and administer epinephrine to restore vascular tone.
- irreversible stage
- the final stage of shock p the multisystem dysfunction that can cause severe cell destruction (may see modeled limbs)
- hypertonic fluid
- a crystalloid used to increase the concentration of the plasma to facilitate movemetn of the interstitial and intracellular fluid into the plasma compartment...into the intravascular space.. need to be concerned c too much fluid overload, CHF especially. effective when a distributive shock is unable to maintain fluid in the vasculature.
- common cellular changes in shock
- decr energy production, deterioration of cellular function, excess production of lactic acid, eruption of the intracellular lysosome, and cell death (decr ATP stores -> no Na-K pump gradient -> K out and Na in -> Na in means H2O enters cell too. can cause swelling and cellular damage
- initial stage
- the first stage of shock when cellular damage occurs b/c not enough o2 is in the periphery. body covers the damage very well and there are no noticable clinical signs.
- plasma expanders
- a colloid solution that contains albumin; hetastarch, dextran, and manitol (man-made molecules that are big and cannot cross membranes, therefore they bring fluid into the vasculature). and the crystalloids (NS, LR, .45NS, and D5W) but can still be used to expand the plasma.
- anaphylactic shock
- a type of distributive shock characterized by massive vasodilation and incr capillary permeability following a severe allergic rxn d/t the inflammatory process and the mast cells of the immune system. the mast cells release vasoactive substances (histamine, serotonin, prostaglandins) which cause vasodilation. anti-histamines, epinephrine, and blood expanders are important to counteract the immune response.