Chapter 15 Flashcards
shock/hypoperfusion
inadequate perfusion of cells, tissue, and organs with oxygen and other nutrients resulting in cell, tissue, and organ dysfunction.
etiology
causation of disease/condition
etiologies of shock
inadequate volume
inadequate pump
inadequate vessel
4 categories of shock
hypovolemic, distributive, cardiogenic, obstructive
5th category of shock
metabolic
hypovolemic shock
low blood volume
most common form of shock
types:
hemorrhagic, nonhemorrhagic, burn
distributive shock
decrease in intravascular volume caused by massive systemic vasodilation and an increase in capillary permeability
types:
neurogenic, septic, anaphylaxis
obstructive shock
results from a condition that obstructs forward blood flow. The volume is adequate, the heart is not damaged, and the vessels are of a normal size with adequate resistance.
cardiogenic shock
caused by ineffective pump function of the heart
metabolic shock
described as a dysfunction in the ability of oxygen to diffuse into the blood, be carried by hemoglobin, off-load at the cell, or be used effectively by the cell for metabolism.
hemorrhagic shock
whole blood from the intravascular space. The term hemorrhagic specifically indicates whole blood loss that can occur from a traumatic injury or a medical illness
nonhemorrhagic hypovolemic shock
caused by the shift of fluid out of the intravascular space; however, red blood cells and hemoglobin remain within the vessels. It is primarily water, plasma proteins, and electrolytes that are lost.
examples:severe diarrhea, vomiting, excessive sweating, and excessive urination.
burn shock
specific form of nonhemorrhagic hypovolemic shock resulting from a burn injury. Burns can interrupt the integrity of the capillaries and vessels and allow them to leak plasma and plasma proteins.
anaphylactic shock
Chemical mediators that are released in the anaphylactic reaction cause massive and systemic vasodilation. These chemical mediators also cause the capillaries to become permeable and to leak.
septic shock
results from sepsis, which is an exaggerated inflammatory response to an infection that causes the vessels throughout the body to dilate and become permeable. Fluid leaks out of the vessels into the interstitial space.
sepsis
the body’s exaggerated inflammatory response to an infection, typically fungal, viral, or bacterial, that overwhelms the body’s normal defense and regulatory systems causing a disruption in cell and organ function.
sepsis pathophsyiology
Increased capillary permeability
Vasodilation
Myocardial depression
Alveolar/capillary membrane damage allowing fluid to accumulate in the alveoli
sepsis s/s
Tachycardia
Tachypnea
Hyperthermia or hypothermia
Hypotension
flushed warm skin (early)
cyanotic (late)
respiratory based sepsis s/s
Productive cough
Fever
Chills
Upper respiratory symptoms (runny or stuffy nose, sneezing)
Throat or ear pain
Crackles upon auscultation (may indicate pneumonia)
GI Based Sepsis s/s
Abdominal pain or flank tenderness
Nausea and vomiting
Diarrhea
Dysuria
Polyuria
robson screening tool
for suspected sepsis
Sepsis is suspected if two of the following findings are present
temp <96.88 or >100.98
hr > 90
RR > 20/min
acute ams
BGL < 120
BAS 90-30-90 scale
for susptected sepsis
Sepsis is suspected if one or more of the following findings are present
systolic bp < 90
RR > 30/min
spo2 < 90
qsofa scale
Sepsis is suspected if two or more of the following findings are present
RR >= 22/min
AMS GCS<13
systolic bp <100
neurogenic shock
Spinal cord injury is a cause of neurogenic shock. A spinal cord injury may damage the sympathetic nerve fibers that control vessel tone below the level of injury. Loss of sympathetic tone causes the vessels to dilate. If the injury is high in the thoracic spinal cord or in the cervical region, enough vessel tone may be lost to cause a drop in systemic vascular resistance, blood pressure, and perfusion.
sympathetic system immediate response to shock
Increase in heart rate
Increase in force of ventricular contraction (stroke volume)
Vasoconstriction
Stimulation of the release of epinephrine and norepinephrine from the adrenal gland
Stages of shock
Compensatory, Decompensatory
Multiple organ dysfunction syndrome (mods)
stage in which multiple organs begin to fail throughout the body from extreme and prolonged hypoxia, altered metabolism, and elevated carbon dioxide and acid levels.
compensatory shock s/s
anxiety
normal bp
mild tachycardia
pulse: thready in extremities
mild-moderate tachypnea 20-30/min
pale cool skin
decompensatory shock s/s
ams
hypotension
marked tachycardia >120
weak/absent pulse
white/waxy skin
hypovelemic shock s/s
decrease bp
narrowing pulse pressure
tachycardia
tachypnea
pale cool clammy skin
poor spo2
weak/absent peripheral pulse
cardiogenic shock s/s
decrease bp
narrowing pulse pressure
tachycardia or bradycardia
tachypnea
pale cool clammy skin
jvd/peripheral edema (R side heart failure)
crackle/rales (L side heart failure)
distributive shock s/s
decrease bp
tachycardia (anaphylactic/septic)
bradycardia (neurogenic)
tachypnea
Flushed skin (sept/anaphylactic)
cyanosis(late sep/anaphy/neuro)
weak/absent pulse
fever (sepsis)
loss of motor function (neuro)
edema (anaphylactic)
obstructive shock s/s
decrease bp
pulsus paradoxus
narrowing pulse pressure
tachycardia
tachypnea
pale cool clammy skin
JVD (tension pneumo, pericardial tamponade)
weak/absent pulse
severely decreased to absent breath sound
Cardiac arrest three phases
electrical, circulatory, metabolic
electrical phase
0-4 min
heart still has a good supply of oxygen and glucose; therefore, aerobic metabolism is maintained with continued energy production for cell function and prevention of mass production of acid.
circulatory phase
4-10 min
the oxygen stores are reduced and the myocardial cells shift from aerobic to anaerobic metabolism. This results in very little energy production for cell function, in addition to the production of acid
metabolic phase
after 10 min
heart is starved of oxygen and glucose and has a large amount of acid buildup. The tissues are ischemic and may begin to die. The chances of survival drop dramatically during this phase
return of spontaneous circulation (ROSC)
when the patient regains a spontaneous pulse during the resuscitation effort. The patient may not yet have begun to breathe on his own
two most common shockable rhythms
Ventricular fibrillation and pulseless ventricular tachycardia
fully automated aed vs semi aed
more buttons to push; semi is more preferred
ventricular fibrillation (v-fib)
a disorganized cardiac rhythm that produces no pulse or cardiac output
pulseless ventricular tachycardia (v-tac)
very fast rhythm that is generated in the ventricle instead of the sinoatrial node in the atrium. Because the pumping is so rapid, the heart does not refill properly and cardiac output is sharply reduced.
non shockable rhythms
asystole and pulseless electrical activity
asystole
absence of electrical activity and pumping action in the heart.
pulseless electrical activity (PEA)
heart has an organized rhythm, but either the heart muscle is so weakened that it fails to pump, or the heart muscle does not respond to the electrical activity, or the circulatory system has lost so much blood that there is nothing to pump.
lateral uterine displacement
relieve pressure off of vena cavae by displacing uterus
women pregnant at 20 weeks or greater
pacemaker aed consideration
dont place pad directly over aed
automatic implantable cardioverter defibrillators (ICDs)
monitor the heart’s electrical activity and provide a shock to the heart if it detects a shockable dysrhythmia
ICD AED Consideration
place pad at least 1 inch away
wait 30 to 60 seconds for the ICD to complete its cycle prior to attaching the AED
