Shock Flashcards
what will happen to O2 supply and demand during shock
- decreased supply and increased demand
- leads to cell death and end organ failure
what is cardiogenic shock
- state when the heart can no longer pump blood forward
left side disfunction of ventricles for cariogenic shock show
- pulmonary edema
- increased preload and after load
right side dysfunction ventricles
- JVD distention
- peripheral edema
- increased preload and after load
- decreased CO and SV
systolic dysfunction
- ineffective forward movement of blood
diastolic dysfunction
- ineffective filling
- increased pulmonary pressures (edema)
hypoxemia is shown by
lowered PaO2 levels
PaO2 levels are:
80-100
- after age 60 you minus 1
pH levels are:
- 7.35-7.45 (7.4 being median)
- if within normal limits if pH is below 7.4 then its more acidic and above more basic
PaCO2 levels are:
- 35-45
- under 35 is basic and over 45 is acidic
what can cause respiratory acidosis
- COPD, over sedation, head trauma
what can cause respiratory alkalosis
- hypoxia, anxiety, PE
Normal HCO3 levels
- 22-26
what causes metabolic acidosis
- ketoacidosis
- lactic acid
- renal failure
- diarrhea
what causes metabolic alkalosis
- fluid loss from GI
- diuretic therapy
- severe hypokalemia (HCO3 gets reabsorbed in kidneys)
common signs and symptoms of cariogenic shock
- tachypnea
- hypotension
- high HR
- decreased urine output
- chest pain (angina)
- eat thready pulse
- pale, cool skin
lab results to look for when cariogenic shock starts
- troponin increases
- BNP and BUN increases
- decreased urine Na
- decreased PaCO2 (alkalosis)
signs and symptoms when left ventricle fails and we see pulmonary edema:
- crackles
- hypoxemia (low PaO2)
- hear S3 and S4
- JVD
- dysrhythmias
signs and symptoms for what happens when compensatory mechanism no longer work during cardiogenic shock (7)
- increased HR
- dysrythmias
- chest pain
- respiratory distress
- respiratory and metabolic acidosis and hypoxemia (increased PaCO2, decreased PaO2 and HCO3)
- renal failure (increased BUN and creation)
- decreased LOC (drop in cerebral perfusion pressure)
pharmacological management for cariogenic shock:
- inotropic agents to increase contractility (dobutamine)
- vasopressors to increase BP (norepinephrine)
- diuretics to decrease preload (lasix)
- antidysrhythmics (amiodarone)
what does inotropic medication do (dobutamine)
- stimulates beta-1 adrenergic
- increase myocardial contractility
- decrease LV pressure
- increases CO without greatly affecting HR
what does vasopressors do (norepinephrine)?
- increases BP and CO
what does lasix do for cariogenic shock
- inhibits reabsorption of Na and Cl
- decreases BP but won’t if used with vassopressures
what are non-pharmacological agents for cariogenic shock
- support ventilation and oxygenation (keep PaO2 above 80)
- support contractility (intraaortic balloon pump)
what is the pathophysiology of hypovolemic shock
- decreased circulation volume
- decreased preload, SV, CO,
- vasoconstriction to fix low BP - increased after load)
- decreased oxygen perfusion and volume supply to organs and tissues
what is absolute hypovolemia
- volume lost from the body
- vomiting, diarrhea
- hemmorage
- diabetes
- hyperglycaemia
- over use of diuretics (diuresis)
what is relative hypovolemic shock
- no loss of volume leaving the body
- move from intravascular space to extravascular space (third spacing)
- vasodilation
class 1/mild hypovolemic shock signs and symptoms (15-20%/ 750mL)
- compensatory mechanisms maintain CO
- mild anxiety
- free of symptoms
- as volume loss increases (vasoconstriction, cool extremities, increased cap refill)
class II/moderate hypovolemic shock signs and symptoms (15-30%/ 750-1500mL)
- decrease CO (more use of comensatory)
- high HR
- increased RR (respiratory alkalosis)
- postural hypotension
- decreased urine output (20-30 mL/h
class III/moderate hypovolemic shock (30-40% or 1500-2000mL)
- compensatory mechanisms begin to fail
- decreased BP
- high HR
- dysrhythmias
- ABG = increased lactate, decreased HCO3 (acidic)
- increased BUN and creation
class IV/severe hypovolemic shock signs and symptoms (greater than 40%) (8)
- no tissue perfusion
- tachycardia
- hypotension
- severe lactic acidosis
- absent peripheral pulses
- cyanotic, severe diaphoresis
- organ failure
- no Urine output
management of hypovolemic shock
- control active blood or volume loss
- initial volume loading
- vasopressors
crystalloid use for hypovolemic shock
- volume expanders
- isotonic or hypertonic
- molecules easily enter extravascular space
- increase preload and SV, CO
colloid solution for hypovolemic shock
- volume expanders
- isotonic or hypertonic
- large molecules can’t enter extravascular space
blood products for hypovolemic shock
- RBC - increase oxygen carrying capacity
- platelets - bleeding due to low platelet count
- frozen plasma - deficient in coagulation factors
Pathophysiology of septic shock
- Vasodilation (low BP, low preload, low afterload, low CO
- decreased tissue perfusion
- inflammation in the blood stream
SIRS
- systemic inflammatory response system
- temp above 38 or less than 36
- HR above 90
- RR above 20 and or PaCO2 less than 32
- WBC - greater than 12000 or less than 4000 (bacteria winning battle)
SIRS
- systemic inflammatory response system
- temp above 38 or less than 36
- HR above 90
- RR above 20 and or PaCO2 less than 32
- WBC - greater than 12000 or less than 4000 (bacteria winning battle)
Antibiotics for septic shock management
- start broad then go narrow once we know what to fight off
Antibiotics for septic shock management
- start broad then go narrow once we know what to fight off
What are the different managements for septic shock
- aggressive fluid resuscitation (increase volume in vasculature)
- antibiotics
- vasopressors (increase BP)
- inotropes (dobutamine) - increase CO and has little effect on HR
- anticoagulants (assess INR before giving)
- control blood glucose levels (continuous infusion of insulin and glucose)
