BCEN Exam - Questions And Precise Solutions (100%)
Compensated Shock Right Ans - Sympathetic nervous system (release of
epi and norepi- vasoconstriction), RAAS activation (inc serum NA and fluid),
ADH (renal NA and H2O absorption) and intracellular fluid shift (inc vasc
volume)
Uncompensated Shock Right Ans - edema/third spacing, respiratory
decline (crackles and dyspnea secondary to pulmonary edema), cardiac
decline (inadequate venous return and dysrhythmias), hypo perfusion to non-
vital tissues, hypo perfusion to myocardium and brain
Hypovolemic Shock Right Ans - Traumatic/nontraumatic hemorrhage, fluid
shift, non-blood fluid losses, urinary fluid losses
Shock Right Ans - impaired tissue perfusion secondary to circulatory
failure
Fluid Volume Intervention Right Ans - crystalloid bolus: NSS is most
common-- 1-2L for adults; 20ml/kg peds
Blood- typically PRBCs (no clotting factors here- just good for volume and O2)
Massive transfusion: 1:1:1 PRBCs, platelets, and plasma
D5W NOT USED- metabolized too quickly and does not contribute to volume
expansion
Cardiogenic Shock Right Ans - Inadequate pump: typically caused by MI,
chest trauma, sustained dysrhythmia, valve problems, end stage
cardiomyopathy
Disruptive Shock Right Ans - Fluid and pump are adequate- but fluid is in
the wrong place (pooling, leaky capillaries)
Types: Anaphylactic, Septic, Neurogenic
Cardiogenic Shock Interventions Right Ans - PEEP (force out pulm edema
fluid)
decrease pre-load (Nitro, MSO4, diuretics, semi-fowlers)
decrease afterload (nitro + antihypertensives)
inc contractility (dobutamine, IABP)
,treat dysrhythmias
Cardiac cath/angioplasty
Anaphylactic Shock Right Ans - Type of Distributive Shock
IGE mediated
IM Epi Q15-20 min
Fluids
Histamine blockers
Albuterol (ensure patent airway)
Corticosteroids
Septic Shock Right Ans - Type of Distributive Shock
Must meet 2 SIRS criteria + known or suspected infection
Considered to be "shock" when pt is hypotensive despite fluid resuscitation
May progress to MODS
Neurogenic Shock Right Ans - Type of Distributive Shock
loss of stimulation of sympathetic (fight or flight) nervous system
(brain/spine injury, spinal anesthesia)
Presents: bradycardia, bradypnea, hypotension, priapism, warm/dry/flushed
skin
Intervention: fluids, vasopressors (phenylephrine), corticosteroids, atropine
Obstructive Shock Right Ans - Hypo-perfusion because of resistance to
ventricular filling
Causes: pericardial tamponade, tension pneumo, PE
Shock in Peds Pts Right Ans - Typically hypovolemia is most common cause
Assess for dryness
Shock in Geriatric Pts Right Ans - Tachycardia may be masked by some
home meds (ie: beta blockers)
Also prone to dehydration/hypervolemia (500 cc bolus followed by 200cc/hr
until SBP 100)
Sepsis is also common cause
Cardiac Output Right Ans - HR influenced by PNS (vagus nerve, drugs,
conduction abnormalities) and SNS (stress, pain)
,Chonotropes Drug Class Right Ans - drugs that affect HR at SA node
Inotropes Drug Class Right Ans - drugs that affect contractility of the heart
Dromotropes Drug Class Right Ans - drugs that affect automaticity
(electrical impulse velocity) at the AV node
Alpha vs Beta Receptors Right Ans - A1 stimulation causes periph vasc
constriction
B2 stimulation causes bronchial smooth muscle dilation
ACE Inhibitors Right Ans - -pril
RAAS system
Decreases preload and afterload
Monitor for cough/angioedema/rash and renal impairment
ARBs Right Ans - -sartan
RAAS system
blocks angiotensin II receptors: vasodilation, decrease aldosterone, inc NA
excretion and sparing K
Only available orally
Monitor for hyperkalemia and hypotension
CA Channel Blockers Right Ans - -dipine
Negative inotropic, chronotropic, and dromotropic effects
Beta Blockers Right Ans - -lol
negative intotropic, chronotropic, and dromotropic effects
Cardioselective: work on B1 (affecting heart rate/contractility/BP and
kidneys by reducing BP via RAAS)
Non-cardioselective: B1 and B2 (B2 affect bronchial smooth muscle and
results in airway dilation)
Nicardipine Right Ans - CA channel blocker, coronary, peripheral
vasodilator
Cont monitoring of BP and HR required
given IV
Labetalol Right Ans - Beta-Blocker
, slows HR, decreases: PVR, CO, BP
moderately decreases preload and afterload
Monitor closely- gradually lower BP to avoid ischemia and infarcts to
brain/heart
Nesiritide Right Ans - BNP
Venous and arterial vasodilator
Continuous monitoring of BP and HR
Given IV
Nitroglycerin Right Ans - Coronary artery dilator (improves collateral
bloodflow to MI tissue)
Peripheral vasodilator: strong pre-load reduction, mild afterload reduction
Must be mixed in glass- may require special tubing
Do NOT give within 24h of phosphodiesterase inhibitors
Nitroprusside Right Ans - Potentiates depolarizing neuromuscular blocking
agents
Decreases SVR
Moderate preload reduction, strong afterload reduction
Caution with hyponatremia, hypothyroidism and renal impariment
Epinepherine Right Ans - Increases CO, HR, SVR and relaxes bronchial
smooth muscle
Titrate to desired response, may cause hyperglycemia
Dobutamine Right Ans - decreases preload and afterload + increases
contractility, SV, and CO Does NOT increase O2 demand
Correct hypovolemia before administering
Dopamine Right Ans - Lower doses: increases contractility
Higher doses: additionally increases vasoconstriction
Correct hypervolemia before administering
Milrinone Right Ans - Increases CO, vasodilation
Decreases SVR
Monitor for dysrhythmias, hypotension, hypokalemia
Norepinepherine Right Ans - Increases CO, HR, SVR
Compensated Shock Right Ans - Sympathetic nervous system (release of
epi and norepi- vasoconstriction), RAAS activation (inc serum NA and fluid),
ADH (renal NA and H2O absorption) and intracellular fluid shift (inc vasc
volume)
Uncompensated Shock Right Ans - edema/third spacing, respiratory
decline (crackles and dyspnea secondary to pulmonary edema), cardiac
decline (inadequate venous return and dysrhythmias), hypo perfusion to non-
vital tissues, hypo perfusion to myocardium and brain
Hypovolemic Shock Right Ans - Traumatic/nontraumatic hemorrhage, fluid
shift, non-blood fluid losses, urinary fluid losses
Shock Right Ans - impaired tissue perfusion secondary to circulatory
failure
Fluid Volume Intervention Right Ans - crystalloid bolus: NSS is most
common-- 1-2L for adults; 20ml/kg peds
Blood- typically PRBCs (no clotting factors here- just good for volume and O2)
Massive transfusion: 1:1:1 PRBCs, platelets, and plasma
D5W NOT USED- metabolized too quickly and does not contribute to volume
expansion
Cardiogenic Shock Right Ans - Inadequate pump: typically caused by MI,
chest trauma, sustained dysrhythmia, valve problems, end stage
cardiomyopathy
Disruptive Shock Right Ans - Fluid and pump are adequate- but fluid is in
the wrong place (pooling, leaky capillaries)
Types: Anaphylactic, Septic, Neurogenic
Cardiogenic Shock Interventions Right Ans - PEEP (force out pulm edema
fluid)
decrease pre-load (Nitro, MSO4, diuretics, semi-fowlers)
decrease afterload (nitro + antihypertensives)
inc contractility (dobutamine, IABP)
,treat dysrhythmias
Cardiac cath/angioplasty
Anaphylactic Shock Right Ans - Type of Distributive Shock
IGE mediated
IM Epi Q15-20 min
Fluids
Histamine blockers
Albuterol (ensure patent airway)
Corticosteroids
Septic Shock Right Ans - Type of Distributive Shock
Must meet 2 SIRS criteria + known or suspected infection
Considered to be "shock" when pt is hypotensive despite fluid resuscitation
May progress to MODS
Neurogenic Shock Right Ans - Type of Distributive Shock
loss of stimulation of sympathetic (fight or flight) nervous system
(brain/spine injury, spinal anesthesia)
Presents: bradycardia, bradypnea, hypotension, priapism, warm/dry/flushed
skin
Intervention: fluids, vasopressors (phenylephrine), corticosteroids, atropine
Obstructive Shock Right Ans - Hypo-perfusion because of resistance to
ventricular filling
Causes: pericardial tamponade, tension pneumo, PE
Shock in Peds Pts Right Ans - Typically hypovolemia is most common cause
Assess for dryness
Shock in Geriatric Pts Right Ans - Tachycardia may be masked by some
home meds (ie: beta blockers)
Also prone to dehydration/hypervolemia (500 cc bolus followed by 200cc/hr
until SBP 100)
Sepsis is also common cause
Cardiac Output Right Ans - HR influenced by PNS (vagus nerve, drugs,
conduction abnormalities) and SNS (stress, pain)
,Chonotropes Drug Class Right Ans - drugs that affect HR at SA node
Inotropes Drug Class Right Ans - drugs that affect contractility of the heart
Dromotropes Drug Class Right Ans - drugs that affect automaticity
(electrical impulse velocity) at the AV node
Alpha vs Beta Receptors Right Ans - A1 stimulation causes periph vasc
constriction
B2 stimulation causes bronchial smooth muscle dilation
ACE Inhibitors Right Ans - -pril
RAAS system
Decreases preload and afterload
Monitor for cough/angioedema/rash and renal impairment
ARBs Right Ans - -sartan
RAAS system
blocks angiotensin II receptors: vasodilation, decrease aldosterone, inc NA
excretion and sparing K
Only available orally
Monitor for hyperkalemia and hypotension
CA Channel Blockers Right Ans - -dipine
Negative inotropic, chronotropic, and dromotropic effects
Beta Blockers Right Ans - -lol
negative intotropic, chronotropic, and dromotropic effects
Cardioselective: work on B1 (affecting heart rate/contractility/BP and
kidneys by reducing BP via RAAS)
Non-cardioselective: B1 and B2 (B2 affect bronchial smooth muscle and
results in airway dilation)
Nicardipine Right Ans - CA channel blocker, coronary, peripheral
vasodilator
Cont monitoring of BP and HR required
given IV
Labetalol Right Ans - Beta-Blocker
, slows HR, decreases: PVR, CO, BP
moderately decreases preload and afterload
Monitor closely- gradually lower BP to avoid ischemia and infarcts to
brain/heart
Nesiritide Right Ans - BNP
Venous and arterial vasodilator
Continuous monitoring of BP and HR
Given IV
Nitroglycerin Right Ans - Coronary artery dilator (improves collateral
bloodflow to MI tissue)
Peripheral vasodilator: strong pre-load reduction, mild afterload reduction
Must be mixed in glass- may require special tubing
Do NOT give within 24h of phosphodiesterase inhibitors
Nitroprusside Right Ans - Potentiates depolarizing neuromuscular blocking
agents
Decreases SVR
Moderate preload reduction, strong afterload reduction
Caution with hyponatremia, hypothyroidism and renal impariment
Epinepherine Right Ans - Increases CO, HR, SVR and relaxes bronchial
smooth muscle
Titrate to desired response, may cause hyperglycemia
Dobutamine Right Ans - decreases preload and afterload + increases
contractility, SV, and CO Does NOT increase O2 demand
Correct hypovolemia before administering
Dopamine Right Ans - Lower doses: increases contractility
Higher doses: additionally increases vasoconstriction
Correct hypervolemia before administering
Milrinone Right Ans - Increases CO, vasodilation
Decreases SVR
Monitor for dysrhythmias, hypotension, hypokalemia
Norepinepherine Right Ans - Increases CO, HR, SVR
