Test 2: Shock Flashcards
MAP
map = DP + 1/3 (SP-DP)
or
map = DP + 1/3(PP)
Normal Map: 60-75mm Hg
CO equation
CO = HR x Stroke Volume
Normal = 4-8 L/min
Total volume perfused per minute
Pulse Pressure
systolic - diastolic
Factors Affecting BP
1) CO, SV, HR (Increase in CO = increase in BP)
2) Viscosity (how thick/thin blood is)
3) Vascular Bed (vasodilation vs vasoconstriction)
Shock
Abnormal metabolism
Systemic Reaction
Syndrome/condition that takes predictable pathway
Life threatening condition due to inadequate tissue perfusion causing possible cell dysfunction, cell death and organ failure
Body tries to compensate
Treatment goal is to intervene in first 1-2 hours before cellular damage occurs
Pathophysiology of Shock
Compensation:
Decrease in BP/MAP
Brain activates SNS to release catecholines - epi/norepi
Vasoconstriction
MAP/BP Increase
Sustained
BP Decreases
BF Decreases (NO O2)
Hypoxemia
Ischemia
Cell Necrosis
LACTIC ACID
Tissue Injury/Death
(repeats LA/Tissue injury)
Organ Failure
Hypovolemic Shock: What is it? What Causes it?
What is it:
Cold shock
LOW BLOOD VOLUME (Decrease BV = Decrease CO, BP/MAP)
Hypoxemia due to decreased perfusion
LOW FLUID VOLUME
Caused By:
Absolute loss/hemorrhagic - trauma, gi bleed, child birth
Relative/nonhemorrhagic - fluid shift from ascites/edema, burns, severe dehydration (vomiting, diarrhea, burns)
Common S/Sx:
Hypotension (<80 systolic) - cold, clammy skin
Tachycardia (>100bpm)
LOW central venous pressure (<2mm Hg)
LOW UOP (<30ml/hr)
Common Interventions:
Priority is hemodynamic stability, increase fluid volume
Lower head of bed to improve blood return - NEVER high fowler/”put the head low in hypovolemic/hypotension”
IV Normal Saline BEFORE vasopressors
Vasopressor - norepinephrine/dopamine
Put SPO2 on forehead
Normal Central Venous Pressure
Normal = 2-6mm Hg
< 2 = threw - need fluid
> 6 = fix - too much fluid
Hypovolemic Lab Profile: pH
7.35-7.45
With hypovolemia we suspect this to decrease and be ACIDIC
Hypovolemic Lab Profile: PaCO2
35-45
With hypovolemia this should be higher
Hypovolemic Lab Profile: PaO2
80-100
Hypovolemia: Decrease
Hypovolemic Lab Profile: Lactic Acid
3-7mg
0.3-0.8
Hypovolemia: Increase
Hypovolemic Lab Profile: HCT
F 37-47
M 42-52
Increase with fluid shift, dehydration
Decrease hemorrhage
Hypovolemic Lab Profile: HgB
F 12-16
M 14-18
Increase fluid shift, dehydration
Decrease hemorrhage
Hypovolemic Lab Profile: K
3.5-5
Increase dehydration, acidosis
Cardiogenic: What is it? Common Causes? S/Sx, Key Treatments
What is it?
- Cold shock
- There is ENOUGH blood but heart not able to pump causing low BP and fluid build up in lungs
- Decrease CO = Decrease BP/MAP
Causes:
CHF
MI
Electrical burn
Dysrhythmia
Hypoglycemia
Acidosis
S/Sx:
JVD
Chest pain
Oliguria (<30ml/hr)
Confusion, Agitation due to decrease BF to brain
Treatment:
- Digoxin for more forceful contraction (HF)
- Dopamine to increase HR, BP (can cause tachycardia/arrythmia
Obstructive Shock: What is it? Common Cause
What is it?
Cold Shock
Physical obstruction preventing blood from moving forward (similar to cardiogenic)
Poor chest recoil - Decrease CO = Decrease BP/MAP
Common Cause:
Cardiac Tamponade (Fluid in heart)
Trauma
Scarring outside chest
Scarring/burns
Pneumothorax
Warm Shock
Caused by inflammatory response which causes vasodilation
Cold Shock
Causes vasoconstriction and cold/clammy
Distributive Shock:
Warm Shock b/c vasodilation
Inflammatory response through entire body
Types:
Neurogenic
Chemical - anaphylaxis or sepsis
Neurogenic Shock: What is it? Caused by? Monitor for?
SCI to T6 or higher
Monitor for s/sx of autonomic dysreflexia
Chemical Shock: Anaphylaxis - what is it? Key treatment?
What is it?
- Severe allergic Reaction
- Allergy introduced - mast and basophils cells released and produce histamine system wide - decreased tissue perfusion
Key Treatments:
#1 Epinephrine (1st) for 1st sign
#2 Diphydreomine (benadryl)
#3 Albuterol
What does histamine cause?
Vasodilation ( decrease CO = decrease bp/map)
Increased HR
Increase capillary permeability causing fluid shift to 3rd space/swelling
Sepsis Shock: What is it? S/Sx? Treatment Priorities?
1 Fluid Replacement
Caused by bacteria, widespread infection or sepsis
Key S/sx:
- Hypotension (<80 systolic, cold clammy skin)
- gi upset
- AMS
- HIGH WBC >10,000
- HIGH TEMP to low temp <96F
Treatment:
#2 Culture
#3 Broad Spectrum Antibiotic
#4 Vasopressors
#5 Sedation to decrease metabolic demand
#6 Medication to prevent ulcer - PPI, H2 block
Initial Stage of Shock: Patho, S/Sx
Patho
Decrease in map by 10 mm Hg BELOW baseline
Anaerobic metabolism w/o S/Sx
“I’m not getting enough pressure” which turns on baroreceptors, brain, SNS/catecholines epi/norepi, vasoconstriction and increase BP
S/Sx:
Increase Diastolic BP (systolic normal)
NARROW PP
Increase HR
Increase RR
Dizziness
Restlessness
Pallor
Common Interventions:
- ABC
- O2 via nasal canula
Compensatory Stage of Shock
- Non-progressive
- Decrease MAP by 10-15mm HG below baseline
- Medical intervention needed to save life
Patho:
SNS Kicks on to increase VS, RAAS kicks on
Decrease BP –> Shunting BF to vital organs –> kidney –> RAAS –> vasoconstriction –>reuptake H20/NA –> UO decrease, Na/K increase
S/Sx:
Decrease UO (declining)
Increase HR
Increase RR
Decrease SpO2
Increase K, NA
Hypoactive BS
Increase Azotemia
Nausea
Progressive Stage of Shock
Decrease MAP by >20 below baseline
Lactic acid >3 is worrisome
LA damaging healthy tissue
Pathophysiology
Decrease BF –> ischemia –> tissue necrosis –> increase LA –> tissue injury –> increase LA –> Mods
S/Sx
Metabolic acidosis
Absent BS
Cheyene Stokes - fast/shallow breathing
Anuria
Increase LA (anything >3 is worrisome)
Decrease SpO2
Increase liver enzymes
Refractory Shock: what is it? S/Sx? Pathophysiology
Poor prognosis
Pathophysiology
Tissue cell death –> increase LA –> cell death –> microthrombi –> decrease bf – ischemic –> tissue necrosis –> increase LA –> cell death
S/Sx:
Bleeding
Ashen
Pupils blown
Mottled
Coma
MODS
DIC
Decrease HR, BP, SpO2
