Shock Flashcards
Shock define
Impairment of perfusion and therefore impairment of cell metabolism
Effects of impaired O2
Less ATP means less NA K pump action
NA influx, then water, so swelling of cells
Membrane potential so less neural or muscular response
Anerobic metab leads to acidosis (end products lactic and pyruvic acid)
Effects of acidosis from lack of O2
Fucks up enzymes
Cell function repair and division stops
Reduces oxygen carrying capacity (curve shift)
Cell and organelle ruptures, lysosomal enzmyes break down cell
Reduced systemic volume causes
Slug cap blood flow so less tissue perfusion so clotting cascade activated which activates inflamm reponse and fluid enters interstitial space
Impairement of glucose use
Increased lipolysis
Increase glycogenlysis
Increased gluconeogensis
Energy costs of these process contribute to cells failure
Problems with glucose impairment
Lipolysis produces ketones causing acidosis
Glycogenlysis requiers energy and H20 to hydrolysis glycogen
Gluconeogensis (glucose from non carbs) uses cell proteins, releases amino acids (acidosis and toxins)
Albumin and other serum proteins broken (loss of vasc volume) protein depletion leads to organ failure
Three mechanisms of shock
Pump failure
Loss of fluid
Loss of PVR
Compensated shock
Negative feedback maintains homeostasis, S&S of shock produces, decreased end organ perfusion happens as comp mechanisms verge on positive feedback (narrowing PP) we begin to see decline to decomp (Hypotsn)
Compensate S&S
Tachy
Peripher vasoconstric (pallor as blood is shunted to organs)
Reduced urine output (saving fluid
NORMAL BP
Decompensated shock
POSITIVE FEEDBACK
Decompensate shock S&S
Hypotensive Tachypnea and SOB (anoxia) Pulmonary edema (heart failing) Oliguria (GFR decreases) Acidosis (kidneys cant excrete) Respiratory acidosis (resp insufficiency causes buildup of CO2)
Irreversible stage of shock
Necrotized parachymal tissue (parachymal is functional part of organs) DIC MODS Circulatory collapse marked hypoerfusion to vital organs Loss of vital functions altered LOC, hypoension, resp distress, acidosis, anuria DIC DEAD AF
Cardiogenic shock
Decreased CO from impaired diastoic filling or obstruction decreased contractility (AMI CHF Cardiomyopathy) Impaired diast (arrhythmias, valve defects) Obstruction (PE, tension pneumo, cardiac tamponade) Most common is AMI
Cardiogenic shock patho
CO drops, renal and hypotalamic reponsed to maintain blood volume (increase preload)
Catecholamines released from adrenals (SVR, contractility, heart rate)
Heart now needs more O2
All mechanisms become positive feedback loop
Clinical manifestations cardiogenic shock
Chest pain JVD classic shock
Etiology of hypovolemic
Loss of volume by
Hemorrhage (whole blood)
Burns (plasma)
Interstitial fluid (sweat, DI, emesis, diuresis)
GI loss (the shits)
Loss of interstistial fluid promotes diffusion of plasma from intravascular to extra vascular, indirectly causing hypovolemia
Hypovolemic numbers
Early 15-25%
Late 30-45%
Catecholamine dump with liver and spleen dumping RBCs
Hypovolemic compensations
Renin stims aldosterone release to retain Na and water
ADH also increases water
Eventually cap hydrostatic pressure drops and interstitial fluid moves into vascular compartments
Clinical manifestations of hypovolemic
Cool pale clammy (high SVR)
Thirst, oliguria, poor skin turgor, prolonged cap refil, tachycardia hypotension
low preloads
3 types of vasogenic shock
Neurogenic
Anaphylatic
Septic
Neurogenic from
Cord or medulla trauma
Conditions interuppting O2 or glucose supply to medulla (insulin reactions or ICP)
Depressive drugs, anesthetic agents, severe emotional stress or pain
Neurogenic patho
Parasympa over stim or sympa under stim
Extreme persistent vasodilation
Neuro shock clinical manifestations
Low SVR
Bradcardia!
High CO still
Anaphylatic shock
IgE mediated hypersensitivty reaction, vasodilation and peripheral pooling
Any antigens
Venoms Pollens shellfish penicillin
Often more severe than others
Immune and inflammatory response to antigen start process
Vasodilation and increased permeability
Constriction of smooth muscle
Similar to neurogenic in major problem is vasodilation
Anaphylactic shock clinical manifestations
Sudden onset, anxiety, dyspnea, edema, GI cramps,hives, pruritis (sense of itching) hypotension, altered LOC, decreased SVR with high or normal CO
oliguria
Septic shock
Complex with rapidly changing clinical manifestations
Starts with septicemia (bactermia) infection, septicemi to SIRS to sepsis to severe sepsis to septic shock
SIRS
Temp over under 36 38
HRT over 90
Resp over 20
Abnormal WBC
Sepsis is
SIRS + infection
Severe sepsis is lactate acid plus sepsis
Septic shock is severe sepsis plus hypotension
Septic shock (high output shock)
Commonly from gram negative bacteria
SIRS causes vasodilation increased permeablilty pooling edema which leads to acidosis and hypoxia severe sepsis means global effects with decreased SVR/preload leading to hypotension and decrease CO
Septic shock pathophysiology
Cell metabolism is impaired by Relative hypovelima from decreased SVR Action of infection agent or Increased O2 from fever CO increases but supply oxygen low from low SVR
Clinical manifestations of septic shock
Varies with inflammatory and immune response
Involvement of varying number of cells, tissues and organs
Similar to neurogenic with increased cap perm and edema
20-90% mortalilty
60% with appropriate antibiotics
