Board of Certification for Emergency Nursing (BCEN) d d d d d d d
Exam Test With Answers [Verified] d d d d
Shock - d d
d d d d d d d d d d d d d d d impaired tissue perfusion secondary to circulatory failure
d d d d d d
Compensated Shock - d d d
Sympathetic nervous system (release of epi and norepi- vasoconstriction), RAAS activation (inc
d d d d d d d d d d d d d d d d d d d d d d d d d d d
serum NA and fluid), ADH (renal NA and H2O absorption) and intracellular fluid shift (inc vasc volume)
d d d d d d d d d d d d d d d d
Uncompensated Shock - d d d
edema/third spacing, respiratory decline (crackles and dyspnea secondary to pulmonary edema),
d d d d d d d d d d d d d d d d d d d d d d d d d d
cardiac decline (inadequate venous return and dysrhythmias), hypo perfusion to non-vital tissues, hypo
d d d d d d d d d d d d d
perfusion to myocardium and brain d d d d
Hypovolemic Shock - d d d
d d d d d d d d d d d d d d d Traumatic/nontraumatic hemorrhage, fluid shift, non-blood fluid losses, urinary fluid losses d d d d d d d d d
Fluid Volume Intervention -
d d d d
d d d d d d d d d d d d d d d crystalloid bolus: NSS is most common-- 1-2L for adults; 20ml/kg peds
d d d d d d d d d d
Blood- typically PRBCs (no clotting factors here- just good for volume and O2)
d d d d d d d d d d d d
Massive transfusion: 1:1:1 PRBCs, platelets, and plasma
d d d d d d
D5W NOT USED- metabolized too quickly and does not contribute to volume expansion
d d d d d d d d d d d d
Cardiogenic Shock - d d d
Inadequate pump: typically caused by MI, chest trauma, sustained dysrhythmia, valve problems,
d d d d d d d d d d d d d d d d d d d d d d d d d d d
end stage cardiomyopathy
d d
Disruptive Shock - d d d
d d d d d d d d d d d d d d d Fluid and pump are adequate- but fluid is in the wrong place (pooling, leaky capillaries)
d d d d d d d d d d d d d d
Types: Anaphylactic, Septic, Neurogenic
d d d
1|Page
,Cardiogenic Shock Interventions - d d d d
d d d d d d d d d d d d d d d PEEP (force out pulm edema fluid)
d d d d d
d decrease pre-load (Nitro, MSO4, diuretics, semi-fowlers)
d d d d d
decrease afterload (nitro + antihypertensives)
d d d d d
inc contractility (dobutamine, IABP)
d d d
treat dysrhythmias d
Cardiac cath/angioplasty d
Anaphylactic Shock - d d d
d d d d d d d d d d d d d d d Type of Distributive Shock d d d
IGE mediated
d d
IM Epi Q15-20 min
d d d
Fluids
Histamine blockers d
Albuterol (ensure patent airway) d d d
Corticosteroids
Septic Shock - d d d
d d d d d d d d d d d d d d d Type of Distributive Shock d d d
Must meet 2 SIRS criteria + known or suspected infection
d d d d d d d d d
Considered to be "shock" when pt is hypotensive despite fluid resuscitation
d d d d d d d d d d d
May progress to MODS
d d d
Neurogenic Shock - d d d
d d d d d d d d d d d d d d d Type of Distributive Shock d d d
loss of stimulation of sympathetic (fight or flight) nervous system (brain/spine injury, spinal anesthesia)
d d d d d d d d d d d d d
Presents: bradycardia, bradypnea, hypotension, priapism, warm/dry/flushed skin
d d d d d d
Intervention: fluids, vasopressors (phenylephrine), corticosteroids, atropine
d d d d d
Obstructive Shock - d d d
d d d d d d d d d d d d d d d Hypo-perfusion because of resistance to ventricular filling d d d d d d
Causes: pericardial tamponade, tension pneumo, PE
d d d d d
2|Page
,Shock in Peds Pts -d d d d d
d d d d d d d d d d d d d d d Typically hypovolemia is most common cause
d d d d d
Assess for dryness d d
Shock in Geriatric Pts -
d d d d d
d d d d d d d d d d d d d d d Tachycardia may be masked by some home meds (ie: beta blockers)
d d d d d d d d d d
Also prone to dehydration/hypervolemia (500 cc bolus followed by 200cc/hr until SBP 100)
d d d d d d d d d d d d
Sepsis is also common cause
d d d d
Cardiac Output - d d d
d d d d d d d d d d d d d d d HR influenced by PNS (vagus nerve, drugs, conduction abnormalities) and SNS (stress, pain)
d d d d d d d d d d d d
Chonotropes Drug Class - d d d d
d d d d d d d d d d d d d d d drugs that affect HR at SA node
d d d d d d
Inotropes Drug Class - d d d d
d d d d d d d d d d d d d d d drugs that affect contractility of the heart
d d d d d d
Dromotropes Drug Class - d d d d
d d d d d d d d d d d d d d d drugs that affect automaticity (electrical impulse velocity) at the AV node
d d d d d d d d d d
Alpha vs Beta Receptors -
d d d d d
d d d d d d d d d d d d d d d A1 stimulation causes periph vasc constriction
d d d d d
B2 stimulation causes bronchial smooth muscle dilation
d d d d d d
ACE Inhibitors -
d d d
d d d d d d d d d d d d d d d -pril d
RAAS system d
Decreases preload and afterload d d d
Monitor for cough/angioedema/rash and renal impairment
d d d d d
ARBs - d d
d d d d d d d d d d d d d d d -sartan
3|Page
, RAAS system d
blocks angiotensin II receptors: vasodilation, decrease aldosterone, inc NA excretion and sparing K
d d d d d d d d d d d d
Only available orally
d d
Monitor for hyperkalemia and hypotension
d d d d
CA Channel Blockers -
d d d d
d d d d d d d d d d d d d d d -dipine
Negative inotropic, chronotropic, and dromotropic effects
d d d d d
Beta Blockers -
d d d
d d d d d d d d d d d d d d d -lol
negative intotropic, chronotropic, and dromotropic effects
d d d d d
Cardioselective: work on B1 (affecting heart rate/contractility/BP and kidneys by reducing BP via RAAS)
d d d d d d d d d d d d d d
Non-cardioselective: B1 and B2 (B2 affect bronchial smooth muscle and results in airway dilation)
d d d d d d d d d d d d d
Nicardipine - d d
d d d d d d d d d d d d d d d CA channel blocker, coronary, peripheral vasodilator
d d d d d
Cont monitoring of BP and HR required
d d d d d d
given IV d
Labetalol - d d
d d d d d d d d d d d d d d d Beta-Blocker
slows HR, decreases: PVR, CO, BP
d d d d d
moderately decreases preload and afterload d d d d
Monitor closely- gradually lower BP to avoid ischemia and infarcts to brain/heart
d d d d d d d d d d d
Nesiritide - d d
d d d d d d d d d d d d d d d BNP
Venous and arterial vasodilator
d d d
Continuous monitoring of BP and HR d d d d d
Given IV d
Nitroglycerin - d d
4|Page
Exam Test With Answers [Verified] d d d d
Shock - d d
d d d d d d d d d d d d d d d impaired tissue perfusion secondary to circulatory failure
d d d d d d
Compensated Shock - d d d
Sympathetic nervous system (release of epi and norepi- vasoconstriction), RAAS activation (inc
d d d d d d d d d d d d d d d d d d d d d d d d d d d
serum NA and fluid), ADH (renal NA and H2O absorption) and intracellular fluid shift (inc vasc volume)
d d d d d d d d d d d d d d d d
Uncompensated Shock - d d d
edema/third spacing, respiratory decline (crackles and dyspnea secondary to pulmonary edema),
d d d d d d d d d d d d d d d d d d d d d d d d d d
cardiac decline (inadequate venous return and dysrhythmias), hypo perfusion to non-vital tissues, hypo
d d d d d d d d d d d d d
perfusion to myocardium and brain d d d d
Hypovolemic Shock - d d d
d d d d d d d d d d d d d d d Traumatic/nontraumatic hemorrhage, fluid shift, non-blood fluid losses, urinary fluid losses d d d d d d d d d
Fluid Volume Intervention -
d d d d
d d d d d d d d d d d d d d d crystalloid bolus: NSS is most common-- 1-2L for adults; 20ml/kg peds
d d d d d d d d d d
Blood- typically PRBCs (no clotting factors here- just good for volume and O2)
d d d d d d d d d d d d
Massive transfusion: 1:1:1 PRBCs, platelets, and plasma
d d d d d d
D5W NOT USED- metabolized too quickly and does not contribute to volume expansion
d d d d d d d d d d d d
Cardiogenic Shock - d d d
Inadequate pump: typically caused by MI, chest trauma, sustained dysrhythmia, valve problems,
d d d d d d d d d d d d d d d d d d d d d d d d d d d
end stage cardiomyopathy
d d
Disruptive Shock - d d d
d d d d d d d d d d d d d d d Fluid and pump are adequate- but fluid is in the wrong place (pooling, leaky capillaries)
d d d d d d d d d d d d d d
Types: Anaphylactic, Septic, Neurogenic
d d d
1|Page
,Cardiogenic Shock Interventions - d d d d
d d d d d d d d d d d d d d d PEEP (force out pulm edema fluid)
d d d d d
d decrease pre-load (Nitro, MSO4, diuretics, semi-fowlers)
d d d d d
decrease afterload (nitro + antihypertensives)
d d d d d
inc contractility (dobutamine, IABP)
d d d
treat dysrhythmias d
Cardiac cath/angioplasty d
Anaphylactic Shock - d d d
d d d d d d d d d d d d d d d Type of Distributive Shock d d d
IGE mediated
d d
IM Epi Q15-20 min
d d d
Fluids
Histamine blockers d
Albuterol (ensure patent airway) d d d
Corticosteroids
Septic Shock - d d d
d d d d d d d d d d d d d d d Type of Distributive Shock d d d
Must meet 2 SIRS criteria + known or suspected infection
d d d d d d d d d
Considered to be "shock" when pt is hypotensive despite fluid resuscitation
d d d d d d d d d d d
May progress to MODS
d d d
Neurogenic Shock - d d d
d d d d d d d d d d d d d d d Type of Distributive Shock d d d
loss of stimulation of sympathetic (fight or flight) nervous system (brain/spine injury, spinal anesthesia)
d d d d d d d d d d d d d
Presents: bradycardia, bradypnea, hypotension, priapism, warm/dry/flushed skin
d d d d d d
Intervention: fluids, vasopressors (phenylephrine), corticosteroids, atropine
d d d d d
Obstructive Shock - d d d
d d d d d d d d d d d d d d d Hypo-perfusion because of resistance to ventricular filling d d d d d d
Causes: pericardial tamponade, tension pneumo, PE
d d d d d
2|Page
,Shock in Peds Pts -d d d d d
d d d d d d d d d d d d d d d Typically hypovolemia is most common cause
d d d d d
Assess for dryness d d
Shock in Geriatric Pts -
d d d d d
d d d d d d d d d d d d d d d Tachycardia may be masked by some home meds (ie: beta blockers)
d d d d d d d d d d
Also prone to dehydration/hypervolemia (500 cc bolus followed by 200cc/hr until SBP 100)
d d d d d d d d d d d d
Sepsis is also common cause
d d d d
Cardiac Output - d d d
d d d d d d d d d d d d d d d HR influenced by PNS (vagus nerve, drugs, conduction abnormalities) and SNS (stress, pain)
d d d d d d d d d d d d
Chonotropes Drug Class - d d d d
d d d d d d d d d d d d d d d drugs that affect HR at SA node
d d d d d d
Inotropes Drug Class - d d d d
d d d d d d d d d d d d d d d drugs that affect contractility of the heart
d d d d d d
Dromotropes Drug Class - d d d d
d d d d d d d d d d d d d d d drugs that affect automaticity (electrical impulse velocity) at the AV node
d d d d d d d d d d
Alpha vs Beta Receptors -
d d d d d
d d d d d d d d d d d d d d d A1 stimulation causes periph vasc constriction
d d d d d
B2 stimulation causes bronchial smooth muscle dilation
d d d d d d
ACE Inhibitors -
d d d
d d d d d d d d d d d d d d d -pril d
RAAS system d
Decreases preload and afterload d d d
Monitor for cough/angioedema/rash and renal impairment
d d d d d
ARBs - d d
d d d d d d d d d d d d d d d -sartan
3|Page
, RAAS system d
blocks angiotensin II receptors: vasodilation, decrease aldosterone, inc NA excretion and sparing K
d d d d d d d d d d d d
Only available orally
d d
Monitor for hyperkalemia and hypotension
d d d d
CA Channel Blockers -
d d d d
d d d d d d d d d d d d d d d -dipine
Negative inotropic, chronotropic, and dromotropic effects
d d d d d
Beta Blockers -
d d d
d d d d d d d d d d d d d d d -lol
negative intotropic, chronotropic, and dromotropic effects
d d d d d
Cardioselective: work on B1 (affecting heart rate/contractility/BP and kidneys by reducing BP via RAAS)
d d d d d d d d d d d d d d
Non-cardioselective: B1 and B2 (B2 affect bronchial smooth muscle and results in airway dilation)
d d d d d d d d d d d d d
Nicardipine - d d
d d d d d d d d d d d d d d d CA channel blocker, coronary, peripheral vasodilator
d d d d d
Cont monitoring of BP and HR required
d d d d d d
given IV d
Labetalol - d d
d d d d d d d d d d d d d d d Beta-Blocker
slows HR, decreases: PVR, CO, BP
d d d d d
moderately decreases preload and afterload d d d d
Monitor closely- gradually lower BP to avoid ischemia and infarcts to brain/heart
d d d d d d d d d d d
Nesiritide - d d
d d d d d d d d d d d d d d d BNP
Venous and arterial vasodilator
d d d
Continuous monitoring of BP and HR d d d d d
Given IV d
Nitroglycerin - d d
4|Page
