Shock

Question 1

Shock define

Answer 1

Impairment of perfusion and therefore impairment of cell metabolism

Question 2

Effects of impaired O2

Answer 2

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)

Question 3

Effects of acidosis from lack of O2

Answer 3

Fucks up enzymes
Cell function repair and division stops
Reduces oxygen carrying capacity (curve shift)
Cell and organelle ruptures, lysosomal enzmyes break down cell

Question 4

Reduced systemic volume causes

Answer 4

Slug cap blood flow so less tissue perfusion so clotting cascade activated which activates inflamm reponse and fluid enters interstitial space

Question 5

Impairement of glucose use

Answer 5

Increased lipolysis
Increase glycogenlysis
Increased gluconeogensis
Energy costs of these process contribute to cells failure

Question 6

Problems with glucose impairment

Answer 6

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

Question 7

Three mechanisms of shock

Answer 7

Pump failure
Loss of fluid
Loss of PVR

Question 8

Compensated shock

Answer 8

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)

Question 9

Compensate S&S

Answer 9

Tachy
Peripher vasoconstric (pallor as blood is shunted to organs)
Reduced urine output (saving fluid
NORMAL BP

Question 10

Decompensated shock

Answer 10

POSITIVE FEEDBACK

Question 11

Decompensate shock S&S

Answer 11

Hypotensive
Tachypnea and SOB (anoxia)
Pulmonary edema (heart failing)
Oliguria (GFR decreases)
Acidosis (kidneys cant excrete)
Respiratory acidosis (resp insufficiency causes buildup of CO2)

Question 12

Irreversible stage of shock

Answer 12

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

Question 13

Cardiogenic shock

Answer 13

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

Question 14

Cardiogenic shock patho

Answer 14

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

Question 15

Clinical manifestations cardiogenic shock

Answer 15

Chest pain JVD classic shock

Question 16

Etiology of hypovolemic

Answer 16

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

Question 17

Hypovolemic numbers

Answer 17

Early 15-25%
Late 30-45%
Catecholamine dump with liver and spleen dumping RBCs

Question 18

Hypovolemic compensations

Answer 18

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

Question 19

Clinical manifestations of hypovolemic

Answer 19

Cool pale clammy (high SVR)
Thirst, oliguria, poor skin turgor, prolonged cap refil, tachycardia hypotension
low preloads

Question 20

3 types of vasogenic shock

Answer 20

Neurogenic
Anaphylatic
Septic

Question 21

Neurogenic from

Answer 21

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

Question 22

Neurogenic patho

Answer 22

Parasympa over stim or sympa under stim

Extreme persistent vasodilation

Question 23

Neuro shock clinical manifestations

Answer 23

Low SVR
Bradcardia!
High CO still

Question 24

Anaphylatic shock

Answer 24

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

Question 25

Anaphylactic shock clinical manifestations

Answer 25

Sudden onset, anxiety, dyspnea, edema, GI cramps,hives, pruritis (sense of itching) hypotension, altered LOC, decreased SVR with high or normal CO
oliguria

Question 26

Septic shock

Answer 26

Complex with rapidly changing clinical manifestations

Starts with septicemia (bactermia) infection, septicemi to SIRS to sepsis to severe sepsis to septic shock

Question 27

SIRS

Answer 27

Temp over under 36 38
HRT over 90
Resp over 20
Abnormal WBC

Question 28

Sepsis is

Answer 28

SIRS + infection
Severe sepsis is lactate acid plus sepsis
Septic shock is severe sepsis plus hypotension

Question 29

Septic shock (high output shock)

Answer 29

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

Question 30

Septic shock pathophysiology

Answer 30

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

Question 31

Clinical manifestations of septic shock

Answer 31

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