Week 4- Shock cardio/obst Flashcards
what is shock
syndrome
- decreased tissue perfusion
- impaired cellular metabolism
results in imbalance between supply and demand of 02 and nutrients
how do we classify shock
based on what caused it
Regardless of the type of shock or what caused it – the end result is
inadequate tissue perfusion due to decreased CO
when cells die…
tissue dies…
when tissues die
organs die
people die
CO=
SV x HR
When we think about shock, we need to think about….
CO
SV includes
preload, afterload and contractility
the amount of blood ejected from the heart with each contraction measured in ml/beat
average normal CO
5000ml/min
how to increase CO
increase HR or SV
shock is an imbalance in
CO
Type of shock impacting preload
Hypovolemic= deals with the loss of volume, from intravascular fluid volume as well as blood loss.
Type of shock impacting Contractility
cardiogenic & obstructive
- ineffective pumping of the heart and insufficient perfusion and delivery of O2 to cells
type of shock impacting afterload (pipes)
Distributive: ineffective distribution of blood volume in the vessels because of vessel dilation and inadequate delivery of oxygen. i.e. sepsis, anaphylaxis, and neurogenic.
Initial phase of shock
- little or no s/s
- lactic acid
compensated stage of shock
classic sign
- fairly normal
- hypotension classic sign late in this stage e
uncompensated (progressive) stage of shock
s/s are obvious
really bad need them out
irreversable or refractory stage of shock
it is over
3 compensatory stage mechanisms
neural: activate SNS epinephrine= increase HR, BP, RR, dilate pupils, broncho dilate, decrease blood flow to kidneys at first
Biochemical: (when acid base comes into play): activated by H+, O2, C02 concentrations. stimulated by HR and RR increase
Hormonal: RAAS, ADH (try to increase BP)
still have adequate CO
neural response
activated by
baroreceptors sense
low pressure and blood flow
biochemical response
chemoreceptors sense: decrease pH, decrease O2 and increase CO2
Angiotensin 2=
Aldosterone=
ADH=
increase afterload and BP
increase preload
increase afterload and BP
S/S of compensated shock
- skin normal or slightly pale, cool peripherly
- ↑ resp. rate; normal WOB, normal SpO2
- thirst
- Slightly restless; possibly mild confusion; decreased concentration, ↑glucose
- mild tachycardia, strong pulse centrally, possibly slightly weaker periphery, normal to low BP
- decreased urine output, urine concentration
what do you want as an order in compensatory shock
3
blood work, lactate, ABG
A client who was in an automobile collision is now in hypovolemic shock. Why is it important for the nurse to take the client’s vital signs frequently during the compensatory stage of shock?
a) Arteriolar constriction occurs.
b) The cardiac workload decreases.
c) Contractility of the heart decreases.
d) The parasympathetic nervous system is triggered.
a
progressive shock
4
- compensatory mechanisms fail
- decreased CO
- Decreased end organ perfusion
- MODS
MODS
- CVS
- Resp
- GI
- Liver
- CNS
- Renal
- skin
- decrease BP, increase HR until gets to tired
- rise in RR, increase WOB, O2 will drop
- nothing, hypoactive bowels
- increase enzymes
- obvious confusion now
- drop in blood flow, decrease UO, increase BUN, Cr
- cold clammy, grey, decreased tissue perfusion, increased cap refill, look sick, green, gross
progressive shock
neuro
CVS
Reps
GI
renal
- confusion obvious, restless, decrease LOC
- pale, cld, clammy, prolonged cap refill, BP, HR decrease
- increase wOB, increase RR, O2 decrease, crackles from shift in fluids
- nothing, nausea/vom (creates pressure to raise BP) decreased bowel sounds
- decreases UO
During the progressive stage of shock, anaerobic metabolism occurs. The nurse expects that initially the anaerobic metabolism causes:
metabolic acidosis
lactate is put out and breakdown is very acidic
refractory shock
loss of compensatory mechanisms
profound cell destruction
organ failure and death
refractory shock
neuro:
CVS:
RESP:
GI:
GU:
DIC
- GCS 4 or 5, not responding, comatose, cerebral edema, extreme decrease in LOC,
- severe decrease CO, major dysrhythmias
- ARDS mixed acidosis, metabolic acidosis because resp is trying to compensate so our resp is pooping out.
- necrotic guts
- anuria
- disseminated intravascular coagulation
bleeding and clotting at the same time
how to intervene refractory stage
- early recognition
- early intervention
systolic dysfunction=
cardiogenic (inability to pump bld fwd)
diastolic dysfunction=
obstructive (↓ RV or LV filling)
obstructive shock usually affects
cardiogenic shock usually affects
Obstructive shock typically just diastole affected
Cardiogenic usually systole and diastole affected
diastolic dysfunction = ineffective filling
increase pulmonary pressures
pulmonary edema
decreased oxygenation
anterior STEMI complications
4
v fib arrest (dysrhythmia)
HF or decreased CO (systole problem)
pericarditis
cardiogenic shock
risk factors for cardiogenic shock from MI
5
age
HTN
DM
Multivessel CAD
Prior MI or Angina
why check BP in both arms
in case of aortic dissection
investigation and management
Orders:
management:
Improve CO:
Orders:
- blood tests: lactate*, CBC, Coags, renal, liver
- ABGs
- Scans
M:
- treat underlying cause (revascularization)
CO:
- increase O2 supply
- decrease O2 demand
- drugs
- LV support
- O2 intubation
drugs for cardiogenic shock
examples and what they do
inotropes*
- (dobutamine (mcg/kg/min)
- milrione
- levophed (norepi)
work more on CO than BP
LV support
reduce myocardial demand
- intra aortic balloon pump (IABP) increase coronary perfusion
- left ventricular assist device (LVAD) - helps bring blood to aorta
pH 7.47
PaCO2 30
HCO3 22
PaO2 98
uncompensated resp alkalosis
Uncompensated is when
Partially compensated is when
Full compensated is when
- CO2 or HCO3 is normal & the other is abnormal
- all 3 are abnormal
- pH is normal
CVP
pressure recorded from the right atrium or superior vena cava and is representative of the filling pressure of the right side of the heart.
High= fluid retention
low=volume depletion, decreased venous tone
pH 7.25
PCO2 30
HCO3 17
PaO2 70
partially compensated metabolic acidosis
hypoxia
pH 7.05
PCO2 56
HCO3 14
PaO2 38
partially compensated mixed acidosis
principles of treatment of shock
1) Treat the underlying cause
2) Increase Supply:
ABC’s
Optimize O2
Optimize CO
Optimize Hgb
3) Decrease Demand:
Normothermia
Decrease Activity
Sedation/analgesia
text book tables
when CO2 high=
When HCO3 high=
acidic
basic
CO2 = acid when high
Bicarb = base when high
