Shock Flashcards
MAP equation
MAP=CO x SVR
SVR determinants
Vessel length, diameter.
Blood viscosity.
Stage of shock
- Pre-shock: (compensated/warm) Hypotension, Peripheral vasoconstriction, Tachycardia.
- Shock: Overwhelmed compensatory mechanism.
S/S end organ dysfxn-Tachycardia, dyspnea, metabolic acidosis, oliguria, confusion, cool clammy skin - End-organ dysfxn: Progressive dysfxn. Irreversibe damage-Coma-Death.
Shock types (5)
- Hypovolemic
- Cardiogenic
- Obstructive
- Neurogenic (injury loss of SNS)
- Distributive (Sepsis, etc. Decreases TVR)
PCWP
Estimates L atrial pressure
Increased: Cardiogenic
Decreased: Hypovolemic & Neurogenic (or normal)
CO
Increased: Early septic (hyperdynamic response)
Decreased: All else (may be normal in neurogenic)
SVR
Increased: Cardiogenic, Hypovolemic, Late Septic (vasodilation)
Decreased: Early septic (vasodilation), Neurogenic
Hypovolumic etiology
- Blood loss (Post-surgical, GI bleed, trauma)
2. Fluid loss (Dehydration, Burns, Acute pancreatitis)
Hypovolumic Pathophysiology
Decreased: blood vol, preload, SV, CO, BP, tissue perfusion
Compensate: Increase SNS, SVR. Blood shunted to vital organs.
Anaerobic metabolism builds Lactate up.
Hypovolumic parameters
- CO decreased
- PCWP/CVR decreased
- TVR increased
Hypovolumic clinical sx
- Greater loss at higher rate=poorly tolerated
- Sx depend on cause
Hematemesis/Melena/Hematochezia
N/V/D
Abdominal pain
Post-op
Hypovolumic PE signs
Dry mucosa
Extremities: cool, clammy, decreased tugor
Decreased BP/JVP/CVP
Increased heart rate
Decreased urine output
Confused mental status
Post-op bleeding-Abdominal pain & distention
Hypovolumic diagnostic tests
- CBC (h&h), CMP, PT/INR (bleeding)
- Lactate (increase assoc with mortality)
- ABG
- Other: CXR, AXR
Hypovolemic treatment
- Treat issue
- Replace volume
Crystalloid/Colloid/Blood (PRBC, FFP, Plts) - Monitor urine, perfusion, mentation
Vasopressor only if SBP<70, dire situation.
(Already vasoconstrict as compensatory)
Cardiogenic/Obstructive etiology
- Ischemia (MI, CM)
- Valve ds (Severe AS, ruptured chordae tendinae/septum)
- Arrhythmia (Vtach/Vfib/Complete heart block)
Obstructive: PE, tamponade, tension pneumothorax
Cardiogenic pathophysiology
Decrease CO, BP,
Decrease renal perfusion-Increase Na/H2O retention
Increase CVP/PCWP-fluid back up in lungs (caution fluids)
Compensatory: Increase SNS, SVR
Cardiogenic parameters
- CO decrease
- CVP/PCWP increase
- TVR increase
Cardiogenic clinical presentation
CP, Dyspnea, Fatigue, Palpitations
Cardiogenic PE signs
Increased JVP, crackles, tachypnea (fluid in lungs) Muffled heart sounds (tamponade) Deviated trachea (tension pneumo) New murmur Cool, clammy extremities
Cardiogenic Dx studies
Same as hypovolumic plus…
Cardiac enzymes (nonspecific)
Echocardiogram
CXR:
Tamponade-enlarged cardiac silhouette
Pneumo-lost vascularity, deviated trachea
Cardiogenic treatment
- Treat issue (cath, ACLS, decompression, pericardiocent)
- Cardio consult
- Caution with fluids (back up into lungs)
- Meds: Inotropes-Dobutamine (increase contractility)
Anti-arrhythmics, diuretics, vasopressors, HF meds.
Last line: LVAD, ECMO, transplant
Distributive etiology
Sepsis Adrenal insufficiency Liver disease Anaphylaxis Drugs/Meds
Septic pathophysiology
Increased O2 demand & Endotoxins
Inadequate perfusion & cell hypoxia
Early septic patho
Vasodilation & hyperdynamic heart
Decreased SVR, BP. Increased CO. Compensates well, but short.
Late septic patho
Vasoconstriction.
Due to hypovolumia (leaking) & decreased BP.
Increased SNS, HR, SVR.
Increased SVR decreases perfusion further.
Sepsis clinical presentation
Increased HR, temp, fever
Decreased BP.
Early-warm. Late-cool.
Confused.
Sepsis Parameters
A) Early
- CO increased
- SVR decreased
- CVR decreased (due to SVR decreasing)
B)
- CO (+/-) usually decreased
- CVR usually decreased (plasma leaking)
- SVR increased
Septic dx studies
Same (including lactate)
+ Blood cultures
Septic treatment
- Goal-directed therapies
- ID problem (culture before AB, Empiric based on likely)
- Fluid
- Vasopressors (NE)
- Ventilator if needed
Septic mortality rate
35-60% 1 mo.
Neurogenic etiology
- Spinal cord injury
2. Brainstem injury (closed head trauma)
Neurogenic pathophysiology
- Unopposed PNS, disrupted SNS
- Decreased HR & SVR (Vasodilation)
- SNS normally released NE/Epi from TL SC
Neurogenic PE signs
- Warm extremities (vasodilations)
- Anal sphincter: decreased tone
- LOC change, Para/quad, DTR increased or gone
- HR normal or gone (ONLY one normal or decrease HR)
- BP decreased
Neurogenic parameters
- CO normal or decreased
- CVR decreased
- TVR decreased
Neurogenic dx studies
- same
- Spinal CT/MRI
- Head CT/MRI
- XR
Neurogenic treatment
Neuro consult!
Address issues, volume replacement.
