Shock Flashcards
Why is hypotension bad
When blood isn’t circulating, there is no tissue perfusion
Give fluid bolus!
What is hypotension vs shock
Hypotension is low blood pressure
Shock is greater oxygen demand than oxygen supply
What can shock lead to
with little tissue perfusion, no oxygen delivery, cellular HYPOXIA and metabolic malfunction
Can lead to cell death; end organ damage; multi system organ failure; death
What is systemic tissue perfusion determined by
MAP= CO x SVR
CO is HR x SV
SVR is influenced by vessel length, diameter, and fluid viscosity
-CO and SVR determine the etiology of shock
What are the stages of shock
Pre-shock: warm, COMPENSATED. tachycardia, perish vasoconstriction, low BP
Shock: compensation OVERWHELMED, signs of organ dysfunction. tachy, dyspnea, metabolic acidosis, oliguria, cold clammy skin
End organ dysfunction: Progressive organ dysfunction, irreversible, coma, death
What are the types of shock
Hypovolemic, Cariogenic, Distributive
Obstructive, Neurogenic
What is an arterial line
line put into radial/brachial/femoral artery to continuously monitor BP and get recurrent ABGs
NOT for meds
What is a central line
placed in vein for delivering critical meds and measuring CVP.
Appropriate for determining fluid status and resuscitation in shock
Can get a triple lumen, double lumen, dialysis cath, Swan-Ganz cath, or PICC line
What is a Peripherally Inserted Central line Catheter (PICC)
Sits on top of the heart, small diameter, can keep for a long time but has increased DVT risk
What is CVP
pressure near the right atrium that correlated “pre-load” or overall volume status. Can be measured with any central line
If CVP is elevated (5-15 mmHg normal), probably don’t want to give many fluids
What is a Swan-Ganz catheter
goes through the RA, RV, and sits in the pulmonary artery. Good for patient in CARDIOGENIC shock
What hemodynamic parameters does a Swan-Ganz measure
Pulmonary capillary wedge pressure (norm 5-15)
Cardiac output (norm 4-8 L)
Systemic vascular resistance (norm 1000-1500)
What is the clinical presentation of all types of shock
Hypotension (SBP <90 or decrease >40)
Tachycardia (except neurogenic shock, brady)
Oliguria
Mental status change (confusion, lethargy)
Metabolic acidosis
Cold clammy skin (except early distributive and neurogenic- warm flushed)
Later: multi organ failure, coagulopathy
What happens in Hypovolemic shock
not enough intravascular volume causes decreased CO and decreased oxygen delivery
What are the causes of hypovolemic shock
hemorrhagic (trauma, GI bleed, internal hemorrhage, post-surgical) Fluid loss (dehydration, n/v/d, burns, acute pancreatitis)
What is the pathophysiology of Hypovolemic shock
decreased blood volume leads to decreased SV
deceased SV leads to decreased CO and BP
decreased BP and volume leads to inadequate tissue perfusion (no oxygen)
Compensation: increased SVR (vessels constrict to shunt remaining blood from periphery to heart, lungs, etc)–baroreceptors sense low BP and activate SNS
Switch to Anaerobic metabolism
What are the hemodynamic parameters of hypovolemic shock
CVP: decreased
CO: decreased
SVR: increased
What does clinical presentation of hypovolemic shock depend on
Amount of blood loss: small is tolerated, large are not
Rate of loss: slow loss allows time for compensation, fast loss leads to shock s/s faster
What do hypovolemic shock patients present with complaints of
Hematemesis, hematochezia, melena N/v/d abdominal pain evidence of trauma Post-op
What are physical signs of hypovolemic shock
Dry oral mucosa
Hypotension, tachycardia, tachypnea, decreased JVP/CVP/urine output
Cold clammy extremities, decreased turgor
Confusion
(May be others with underlying pathology)
What diagnostic studies are needed for Hypovolemic shock
CBC, CMP, PT/INR (are they bleeding?) Lactate (marker of tissue perfusion, increase during ANaerobic perfusion) ABG CXR/ chest CT Abd XR/CT
What is increased lactate associated with
increased mortality
if high, there is not enough tissue perfusion
How do you manage hypovolemic shock
REPLACE VOLUME: crystalloid (saline), Colloid (albumin), blood (PRBC, FFP, Plts)
If SBP <70, can use vasopressors while restoring volume (emergency)
What should you monitor when managing hypovolemic shock
urine output, peripheral perfusion, mentation
What is Cariogenic shock
decreased CO due to pump failure
What are the etiologies of cariogenic shock
Ischemia (MI, cardiomyopathy)
Valvular HD (ruptures pap muscle/chords, ventricular septum rupture)
Arrhythmias (VFib, VTach, complete heart block, AFib, Aflutter)
Obstructive (extra cardiac)- massive PE, cardiac tamponade, tension PTX
What is the pathophysiology of cariogenic shock
Bad pump causes decreased BP and CO
decreased BP/CO turns SNS on, and cause decreased renal perfusion
decreased renal perfusion causes sodium and water retention (RAAS)
Increased filling pressure (CVP) causes volume overload in lungs (pulm edema)
Compensation: increased SVR
What are the hemodynamic parameters in Cariogenic shock
CVP: increased
PCWP: increased
CO: decreased
SVR: increased
What is the clinical presentation of cariogenic shock
CP
Dyspnea
Palpitations
Fatigue
What are the physical signs of cariogenic shock
tachycardia, tachypnea, hypotension cool clammy extremities increased JVP muffled heart sounds, new murmur, tachycardia deviated trachea crackles if with pulmonary edema
What diagnostic studies would you get for cariogenic shock
CBC, CMP, cardiac enzymes, ABG, ECG, CXR, Echo, CT chest
How do you manage cariogenic shock
treat underlying problem! --MI- oxygen, cath lab --VTach/VF- ACLS --tension PTX- decompression --cardiac tamponade- pericardiocentesis Cardio consult Fluids (VERY cautious, fluid overload)
What meds may be provided in the management of cariogenic shock
Inotropes (Dobutamine 1st, +/- vasopressors)
diuretics
anti-arrhythmatics
HF meds
What is your last resort in cariogenic shock management
Assist devices (LVAD, RVAD, artificial heart)
ECMO
Heart transplant
What are the causes of distributive shock
SALAD Sepsis Adrenal Insufficiency Liver disease Anaphylaxis Drugs/meds
What are the types of vasodilator shock
Distributive and neurogenic shock
What is septic shock
inadequate tissue perfusion and oxygen supply when tissues require more while combating systemic infection and septic endotoxins (increased metabolic needs while fighting an infection)
-any kind of infection; UTI, PNA, bacteremia, etc.
What is “early septic shock”
Vasodilation- initial response to meet increased oxygen needs (HYPERDYNAMIC response)
Well compensated, but difficult to maintain
Start to see signs of organ impairment due to endotoxins aggravating cellular hypoxia
What is the stampede analogy in early septic shock
pro-inflammatory cells outnumber anti-inflammatory cells (malignant intravascular inflammation) causing profound vasodilation
What is “late septic shock”
start to see cap leakage and loss of vascular tone, leading to HYPOvolemia and HYPOtension. Cant compensate anymore
Vasoconstriction is worse for present hypoxia and causes organ system malfunction (poor perfusion to extremities and internal organs)
What is the clinical presentation of septic shock
fever, hypotension, tachycardia
warm (early) extremities, then cold (late)
confusion
What clinical features in elderly/immunocompromised make you suspect septic shock
unexplained hypotension, mental status changes, signs of organ dysfunction
What are the hemodynamic parameters of early shock
CVP: decreased (vasodilation)
CO: increased
SVR: decreased (vasodilation
What are the hemodynamic parameters of late shock
CVP: usually decreased (can be increased)
CO: decreased
SVR: increased
What diagnostic studies are important for septic shock
LACTATE! CBC/CMP Cultures ABG CXR
How do you manage septic shock
early goal directed therapy is beneficial
Treat underlying problem; Panculture BEFORE abx, then abx empirically until results come back
FLUID!!
What meds assist in septic shock management
Vasopressors (norepinephrine)
What further management options are there for septic shock
ventilator support if indicated (PNA, labored breathing)
What is neurogenic shock
loss of sympathetic tone leading to vasodilation and hypotension
BRADYCARDIA! (loss of SNS kicks PNS up)
What is the etiology of neurogenic shock
spinal cord injury (disruption between brain and spinal cord)
closed head trauma w/ brainstem injury
What happens to the SNS in neurogenic shock
- Sympathetics usually leave brain stem, down C-spine, exit TL region and release epi/norepi (increased HR, contractility, vasoconstriction)
- Disruption of SNS results in unopposed PNS= hypotension, decreased SVR, and normal/bradycardia
What is the clinical presentation of septic shock
HR normal or brady \+/- altered LOC para-quadriplegic absent DTR/hyperreflexia warm extremities (vasodilation) decreased sphincter tone (PNS)
What are the hemodynamic parameters in septic shock
CVP: normal or low (hypotension)
CO: normal or low (decreased HR)
SVR: decreased (vasodilation)
What diagnostic studies would you get for septic shock
CBC, CMP
C-spine XR (C7-T1)
Head CT (r/o structural lesions, shift, herniation)
Spine CT/MRI
How do you manage septic shock
fluids to correct HYPOvolemia
Neurosurg consult asap
