Flashcards in Shock and Resuscitation Deck (38)
Characteristics of hypovolemic shock?
SVO2: low or normal
cold, clammy b/c increased SVR, slow cap refill
- think trauma and hypovolemia - hemorrhagic until proven otherwise, don't transfuse until Hgb less than 7, unless deteriorating quickly
- give warm fluids, blankets, correct coag (give PRBCs, platelet,s FFP)
Characteristics of cardiogenic shock?
pp: decreased, cold clammy
- have to figure out underlying cause, don't overload w/ fluids
Characteristics of distributive shock?
- CVP: low (+/-)
- PWCP: low (+/-)
- SVO2: high (+/-)
- SVR: really low
- CO: high (+/-)
- PP: wide (diastolic typically goes down), warm extremities (SVR low)
- can be sepsis: tx w/ fluids and empiric abx
- anaphylaxis: fluid bolus asap, epi
- adrenal crisis: fluids, steroids
- neurogenic: dx of exclusion, tx bradycardia
Characteristics of obstructive shock?
- CVP: +/-
- PWCP: +/-
- SVO2: +/-
- SVR: high
- CO: low
- want echo, ekg, CXR to dx underlying cause
- give IV fluids to raise pressure, desat quickly
tension pneumo - thoracostomy
DDx for crashing pt?
Indicators of shock?
- can't always base off of BP
- are tissues perfusing? skin changes
- hypotension, tachycardia
- tachypnea early indicator
- metabolic derangements: lactic acid, AGMA, BUN/Cr, transaminasess, coag factors, changes in SVO2, ScVO2
Cause of hypovolemic shock? H and P findings?
- someone left the valve open
- loss of intravascular vol:
hemorrhage, GI/GU losses, dehydration, decreased filling pressures/CO, high SVR (reflex vasoonstriction), decreased SVO2/ScVO2
- H and P:
diarrhea, polyuria, poor intake, obvious volume loss (exsanguination), flat, non-distended neck veins
Effects of 15% loss of blood?
- HR minimally elevated or normal, no change in BP, PP, or RR
- orthostatic hypotension
Effects of 15-30% loss of blood?
- tachycardia (100-120)
- tachypnea (RR 20-24)
- decreased PP
effects of more than 40% blood loss?
- sig depression in BP and mental status
- PP narrowed less than 25 mmHg
- tachycardia over 120
- urine output: minimal or absent
- skin cold, pale, cap refill is delayed
- will have supine hypotension
The triad of death?
- coag leads to metabolic acidosis (lactic acidosis) - leads to hypothermia (decreased myocardial performance - leads to halt coag cascade - coag and repeat
What is recommended for severe ongoing hemorrhage?
- immediate transfusion of blood products in 1:1:1 ratio of PRBC, FFP and platelets.
What is cardiogenic shock, H and P findings?
- pump is broken
- failure of heart to provide forward flow:
ischemia, cardiomyopathy, mechanical, arrythmia
- High SVR, high filling pressures, low CO
- low SVO2/ScVO2
- H and P:
chest pain, orthopnea/PND, EKG
JVD, periph/pulm edema, S3 gallop
Tx of cardiogenic shock?
- goal: improve CO while reducing myocardial workload
- be careful w/ IV fluids
- consider inotropic and/or vasopressor support
- management of underlying causes:
revasc, rhythm conersion, HF optimization
What is distributive shock? H and P findings?
- pipes are the wrong size
- decrease in syst. vascular tone:
-loss of fluid into extravascular 3rd space
-sepsis, neurogenic injury, anaphylaxis, adrenal crisis
-low SVR (vasodilation)
-low filling pressures, high CO initially (hyper dynamic)
-SVO2/ScVO2 nomal or high
- H and P:
known allergy, spinal injury, fever/infectious sxs, warm, edematous extremities
Tx of anaphylactic shock?
Can be rapidly fatal
- IV fluid boluses, IV antihistamines, IV corticosteroids
- actively search for/remove offending allergen
- IM epi (1:1000) in 0.3-.5 mg doses necessary to maintain perfusion
refractory pts: 0.3-0.5 mg doses of IV epi (1:10,000) given over 2-3 min
Tx of adrenal crisis caused distributive shock?
- difficult to determine appropriateness of cortisol levels in seriously ill pt
- support hemodynamics w/ IV fluids, pressors as necessary
- stress dose steroids (hydrocortisone)
- dx of exclusion
- IV fluid resuscitation
- pressor support for failed response
- atropine, dopamine, transcutaneous pacing necessary for bradycardia
What is obsructive shock?
- stopped pipe
- impaired cardiac filling:
-absence of pressure gradient in R heart
-decrease in venous return
-cardiac tamponade, pericarditis, tension pneumo, PE
-high filling pressures, low CO, high PVR/SVR
- H and P:
becks triad, asymmetric breath sounds, friction rub
- pulsus paradoxus
Causes of obstructive shock?
- cardiac tamponade:
IV fluid, emergent pericardiocentesis
- PE: IV fluid, vasopressor support (NE), avoid inubation if possible, thrombolytics (CIs?)
- tension pneumo: IV fluid, emergent needle thoracostomy followed by chest tube
General principles of resuscitation?
- hemodynamic/ventilatory support:
improve components of O2 delivery/consumption
- decrease tissue metabolic demands: consider early mechanical ventilation, hyperactive resp muscles can steal up to 50% of cerebral blood flow
- primary need is to restore normal cellular fxn
Monitoring for pts in shock?
need to be admitted to ICU:
- high risk of decompensation
- BP (invasive)
- pulse ox
- mental status
How can we max O2 delivery? When should we transfuse?
- supp O2, positive pressure ventilation:
allows for improved oxygenation, also reduces O2 demand by reducing WOB
- transfusion parameters:
at 7 unless cardiac ischemia
Describe the inability to match metabolic demands?
- O2 delivery/consumption mismatch
- under normal circumstances:
O2 consumption is 250 cc/min
What should be given if pt's hypotension is refractory to IVF?
- inotropes and vasopressors
Receptors and fxns?
- B1: increases cardiac contractility/chronicity
- B2: induces smooth muscle vasodilation
- a1: arterial vascular smooth muscle contraction
- D1/D2: vasodilation of renal/splachnic vasculature
- most affect a mult. of receptors
MOA of NE?
- primarily a1 agonist (some inotropic effects as well)
- vasoconstriction w/o impacting CO or HR
- 1st line for septic shock, also recommended in undiff shock states
- can be toxic to cardiac myocytes (apoptosis)
MOA of Vasopressin?
- acts on V1(vasc)/V2(renal) receptors:
V1 stim smooth muscle contraction, V2 increases water resorption at collecting ducts
- improves sensitivity to NE
- not affected greatly by acidosis/hypoxia
MOA of dopamine?
- natural precursor to NE
- affects diff receptors at diff doses:
3-10 micrograms/kg/min: B1 (promotes NE release)
10-20micrograms: a1 (vasoconstriction)
- assoc w/ higher risk of tachyarrhythmias