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Types of shock
- Hypovolemic
- Transport
- Obstuctive
- Cardiogenic
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3 Physiologic issues w/ Hypovolemic shock
- Volume decrease
- Intravascular compartment increased (vessel size)
- Reduced ventricular filling pressure, SV, CO, and BP
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Causes of volume loss
- Hemorrhage
- Dehydration
- Burns
- Vomiting: losing fluid and decreased intake bc vomiting
- Diarrhea
- 3rd spacing
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Causes of increased intravascular compartment
- Vasodilation: neurogenic shock, spinal cord injury, anaphylactic shock (allergic rx), septic shock (dilated and fluid in 3rd spaces)
- Paraplegics' legs do not get signal to vasocontrict
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Sepsis
- Must meet 2 criteria
- Temp: >100.4 or <96.8
- HR: >90
- RR: >20
- WBC: >1200, <4000, or >10% band cells
- BP is not an indicator!
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Severe Sepsis
- Sepsis PLUS at least one criteria
- Acute Organ dysfunction: at least one
- Hypoperfusion
- Hypotension: lactic acidosis, oliguria
- Acute LOC alteration
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Septic Shock
- Persistent Sepsis-Induced hypotension: despite adequate fluids
- MODS
- Persistent shock state
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Transport shock causes
- Hemorrhage
- Anemia
- Carbon monoxide toxicity: has greater affinity than O2
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Obstructive shock causes
- PE: V/Q perfusion mismatch, increased pulmonary vascular resistance
- Tension pneumothorax: impedes venous return
- Cardiac tamponade: impairs ventricular filling and decreases CO
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Cardigenic Shock: R vs. L
- Right: ventricle fails to pump necessary volume
- Left: ventricle fails to pump oxygenated volume
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Cardiogenic Shock causes
- Massive MI (#1)
- Acute Mitral Valve regurgitation
- Cardiomyopathy: so large that beomces ineffective, can't squeeze well
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Cardiogenic Shock at risk populations
- Elderly
- Diabetic
- Anterior MI
- Previous MI
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4 Stages of shock
- Initial
- Compensatory
- Progressive
- Refractory
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Initial Stage of Progression
- Decreased O2 delivery leads to anaerobic metabolism and lactic acidosis
- Want to catch here
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Compensatory Stage of Progression
- Neuroendocrine reponses are activated and clinical s/s can be seen
- Kidneys retain, HR increases, CO increases, LOC changes
- Looks for trends
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Progressive Stage of Progression
MODS
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Refractory Stage of Progression
- Cell destruction and death
- Resistance to conventional therapy
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Clinical findings in shock
- BP, HR, UOP, RR (compensatory)
- Lactate levels: measure of impaired O2 and hypoperfusion
- Base Deficit: the amt. of bicarb/base the body needs to raise one liter of blood to normal pH
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Clinicals Signs in hypovolemic shock
- VS: decreased BP (orthostatic), increased HR, decreased UOP
- Hemodynamics: decreased PAP PAQP and CO, increased SVR (compensation vasocontriction)
- Skin: cool, poor cap refill
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Clinical signs in neurogenic shock
- VS: decreased HR
- Hemodynamics: decreased SVR, CO, RAP, PAP, PAWP
- Skin: warm, no sweating below level of spinal cord injury
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Clincal signs of anaphylatic shock
- Erythema
- Urticaria
- Pruritis
- Angioedema
- Dyspnea
- Wheezing
- Feeling warm
- Laryngeal edema
- Severe bronchoconstriction w/ stridor
- Decreased LOC
- Common, develops w/in 5-30mins but can take as long as 6-12hrs
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Early/Late S/S of septic shock
- Early: Changes in LOC, increased RR, fever or hypothermia
- Progressive: fluid shifts (3rd spacing and edema), increased WBCs, positive blood cultures, pulmonary infiltrates, normal or increased CO/CI, decreased bowel sounds (perfusion issue, protects heart and lungs first), ischemia/necrosis of extremities (fibrinolytic response), coagulopathy (bleeding from insertion sites, prolonged bleeding time, altered platelet count; compromised liver)
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Clinical signs of transport shock
- Low HCT
- Low to normal RAP and PAWP: depends of body's ability to compensate
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Transport shock: carbon Monoxide s/s
- HA
- Malaise
- Nausea
- Memory loss
- Personality changes
- Neurologic dysfunction
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Clinical signs of Obstructive shock
Pulsus Paradoxus: a decrease of >10mmHg of the SBP during inspiration
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ABGs for shock
will see metabolic acidosis initially because of lactic acid
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Treatment: Optimize O2 delivery
- Supplemental O2
- IV fluids: LR, blood for low HCT, albumin for normal HCT
- Inotropic med: dopamine, dobutamine, milrinone; use w/ caution, can exacerbate problem if valuves aren't working or demand is too high
- Vasocontrictors: epinephrine, norephinephrine (levophed), vasopressin
- Vasodilators: nitroprusside, nitroglycerin; decreases afterload
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Treatment: Minimize O2 Consumption
- Decrease total body work
- Decrease pain
- Decrease anxiety
- Decrease temp
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Treatment: Specific Options
- Treat hypersensitivity rx: antihistamines (Benadryl), Bronchodilators (albuterol)
- Low-Dose Steroids: body needs this to help drive compensatory mechanisms
- Restore balance b/t coag and fibrinolysis: Xigris (extreme cases)
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