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80 Cards in this Set

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what is the definition of hemodynamic monitoring?
the study of physical factors regulating blood flow
what is the purpose of hemodynamic monitoring?
1. to measure cardiovascular performance
2. to assess etiology of shock states (hypoperfusion and organ dysfunction)
what are the five hemodynamic components?
BP - blood pressure
MAP - mean arterial pressure
CO - cardiac output
CI - cardiac index
SVR - systemic vascular resistance
How is MAP calculated?
2/3 diastolic BP + 1/3 systolic BP = MAP
Blood pressure: what is it, what is it associated with, how is it calculated?
BP is the pressure of blood against arterial walls
It is associated with oxygen delivery and tissue perfusion
BP = CO x SVR
CO and SVR are balanced in order to maintain BP
Cardiac output: what is it and how is it calculated?
CO is the volume of blood ejected per minute (L/min)
CO = SV x HR
what three factors affect stroke volume?
preload, afterload, contractility
what is preload? how is it estimated?
preload: how much blood is going to the left ventricle
LVEDV is estimated by the PCWP (the volume right before systole)
what is afterload? how is it estimated?
afterload: resistance of the left ventricle
it is estimated by SVR
what is the term used to describe contractility?
inotropy
what is cardiac index and how is it calculated?
CI: normalization of CO to body size
CI = CO/BSA
what are some non-invasive measures of hemodynamics? (3)
vital signs (BP, HR)
pulse oximetry (PaO2)
transthoracic echocardiogram (TTE) - measures ejection fraction
what are some invasive measures of hemodynamics? (3)
arterial line (PaO2)
central venous catheter (meaures BP - fluid status of the venous side)
pulmonary arterial catheter
describe the frank starling mechanism
increases in venous return to left ventricle will increase left ventricular end diastolic pressure (LVEDP) and volume, thereby increasing preload. this resutls in an increase in stroke volume. in a normal heart, at a certain LVEDP further increases in pressure/volume will NOT cause an increase in stroke volume. in a failing heart, this happens at a much lower LVEDP
what is a pulmonary arterial catheter useful for?
volume status
ventricular performance
estimating Oxygen delivery and uptake
can help differentiate between shock syndromes
true or false: use of a PAC will decrease mortality
false: use of a PAC will cause no difference in mortality
what are some potential adverse effects of using a PAC?
it can lead to premature atrial or ventricular contractions and pulmonary artery rupture
which direct measurements and calculated measurements can a PAC be used to obtain?
direct:
CVP - central venous pressure
PAP - pulmonary artery pressure
PCWP - pulmonary capillary wedge pressure
CO - cardiac output
SVO2 - mixed venous oxygen saturation
calculated:
SV
CI
SVR
LV stroke work index (LVSWI)
what is the normal value for CO?
4-7 L/min
what is the normal range for CI?
2.8-4.5 L/min/m2
what is the normal range for SV?
60-100mL
what is the normal range for SVR?
900-1400 dynes*sec/cm5
what is the normal range for PCWP?
6-15 mmHg
what is the normal range for CVP?
2-6 mmHg
what is the normal range for MAP?
80-100 mmHg
matching:

CVP preload
CI fluid status
SVO2 organ perfusion
MAP cardiac inotropy
PCWP oxygen consump.
CVP = fluid status
CI = cardiac inotropy
SVO2 = oxygen consumption
MAP = organ perfusion
PCWP = preload
assess the following clinical situation:
pts CI is 1.5 and PCWP is 10
hypovolemic shock
assess the following clinical situation:
pts CI is 1.5 and PCWP is 23
cardiogenic shock
assess the following clinical situation:
pts CI is 3 and PCWP is 12
normal
assess the following clinical situation:
pts CI is 3 and PCWP is 25
pulmonary edema
what are the goals of pharmacologic therapy in managing hemodynamic instability?
increase tissue perfusion:
increase MAP >65 mmHg
increase CO
normalization of oxidative metabolism:
return of aerobic metabolism (hypoperfusion leads to anaerobic metabolism which leads to acidosis)
what are the categories of fluids and what are some examples of each?
crystalloids: Normal saline (NS) and lactated ringers (LR)
colloids: albumin 5% and hetastarch 6%
blood
what are the advantages of using crystalloids?
low cost
widely available
what is one advantage to using lactated ringers?
the bicarbonate is good for pts w/ acidosis
what is a disadvantage to using crystalloids?
only 25-33% remain in intravascular space
when giving fluids, what compartment do we want it to stay in?
intravascular - plasma
what is an advantage to using colloids?
80-100% remain in intravascular space
what are some disadvantages to using colloids?
very expensive
may not be readily available
what types of blood products are used in treating hemodynamic instability?
whole blood
packed red blood cells (PRBC)
platelets
crypoprecipitate (clotting factors)
when is the use of blood products indicated in pts w/ hemodynamic instability?
only if Hgb is decreased or if there is a loss of blood
what are the treatment goals when administering fluids to a hemodynamically unstable pt?
maintain adequate circulation for tissue perfusion:
MAP > 60-65 mmHg
SPB > 90 mmHg
CI > 2.2 L/min/m2
additional markers of adequate perfusion:
normal heart rate (<90bpm)
adequate UO (>0.5-1 mL/kg/hr)
what is the physiologic and hemodynamic effect of stimulating a1 receptors?
physiologic: arterial and venous vasoconstiction
hemodynamic: increase in SVR and MAP
what is the physiologic and hemodynamic effect of stimulating B1 receptors?
physiologic: increase in contractility and chronotropy
hemodynamic: increase in CO and HR
what is the physiologic and hemodynamic effect of stimulating B2 receptors?
physiologic: arterial and venous vasodilation
hemodynamic: decrease in SVR
what is the physiologic and hemodynamic effect of stimulating DA receptors?
physiologic: vasodilation
hemodynamic: ? increase in UO?
what is the physiologic and hemodynamic effect of stimulating VP receptors?
physiologic: vasoconstriction, fluid retention, increase in cortisol
hemodynamic: increase in SVR and MAP
classify the following agents as either vasopressors (increase SVR) or inotropes (increase in CO): dopamine, dobutamine, vasopressin, norepinephrine, milrinone, levosimendan, epinephrine, phenylephrine
vasopressors: dopamine, norepinephrine, epinephrine, phenylephrine, vasopressin
inotropes: dopamine, dobutamine, milrinone, levosimendan
Dopamine works on which receptors?
DA, B1, a1
what dose of dopamine is used for stimulating DA receptors and what is the effect?
0.5-3 mcg/kg/min
increases renal and mesenteric blood flow, mesenteric/renal/cerebral/coronary arterial dilatation, ? increase in UO?
what dose of dopamine is used for stimulating B1 receptors and what is the effect?
3-10 mcg/kg/min
increase inotropy (contractility) and chronotropy (HR), increase CO
what dose of dopamine is used for stimulating a1 receptors and what is the effect?
10-20 mcg/kg/min
incease in peripheral vasoconstriction, SVR, MAP
what effect dose dopamine have on renal tubules?
inhibits proximal tubule sodium reabsorption
Dopamine stimulates the release of ______________?
norepinephrine
true or false: renal dose dopamine decreases mortality of critically ill pts by preventing acute renal failure
false: renal dose dopamine should never be used
what adrs are associated with dopamine?
tachyarrhythmia
increased afterload and preload
increased myocardial oxygen demand (can cause MI)
peripheral ischemia
pulmonary congestion
Norepinephrine stimulates which receptors and causes what effects?
a1 receptors: increase peripheral vasoconstriction (increase SVR)
negligible B effects
what effect does pH have on NE? why is this important?
decreased activity in acidosis, may need to increase dose; if organs are not perfused, may lead to anaerobic metabolism - leads to acidosis
what is the normal dosing range of NE?
2-50 mcg/min (max 200); dose titrated to MAP > 65 mmHg
what ADRs are associated w/ NE?
increased afterload
cardiac arrhythmias
peripheral ischemia
increased myocardial oxygen demand (not as much as DA)
phenylephrine stimulates which receptors and causes what effects?
stimulation of a1 receptors: increase in peripheral vasoconstriction
no B effects (no increase in myocardial oxygen demand)
what is the normal dosing range of phenylehprine?
30-300 mcg/min (max 200) titrated to MAP >65 mmHg
what ADRs are associated w/ phenylephrine?
increased afterload
reflex bradycardia
peripheral bradycardia
peripheral ischemia***
myocardial ischemia
hypertension
why is phenylephrine considered second line?
extreme peripheral ischemia - may lead to amputation
why should pressors be d/c's ASAP?
they can cause peripheral ischemia
epinephrine works on which receptors and causes what effects?
stimulation of a1 receptors: increase peripheral vasoconstriction
stimulation of B receptors: increase in inotropy/chronotropy, increase in peripheral vasodilation
(effects are dose dependent)
what are the normal doses for epinephrine?
B1, B2: 0.01-0.05 mcg/kg/min - increase in SVR/MAP
a1, B1: >0.05 - increase in CO, HR, contractility
what are the ADRs associated w/ epi?
increased in myocardial ox demans
tachyarrhythmias
ischemia
lactic acidosis
what receptors does vasopressin stimulate? what are the effects of each?
VP1: peripheral vasoconstriction
VP2: sodium and water retention, decreased UO
**VP3: increase ACTH and cortisol production
when is vasopressin used and what is the benefit?
used in adjunct to other pressors in septic shock. benefit= you can decrease the dose of other pressors when you add vasopressin
what is the normal dosing of vasopressin?
0.01-0.04 units/min
what are the ADRs associated w/ vasopressin?
decrease CO
myocardial and splanchnic ischemia (necrotic bowel)
what receptor does dobutamine stimulate? what is the effects?
B receptor: increase inotropy/chronotropy, increase CO
a1 receptor: minimal - increase in peripheral vasoconstriction (smaller effect than B1 effects)
what is the normal dosing of dobutamine?
2.5 mcg/kg/min (max 20 mcg/kg/min) titrate to desired CI
what are the ADRs associated w/ dobutamine?
ventricular arrhythmia
hypotension (usually does cause this)
increase myocardial O2 demand
when is dobutamine C/I?
SBP < 100mmHg
what is the moa if milrinone? what is its effects?
MOA: PDE-3 inhibitor - inhibits breakdown of cAMP in myocardium and vasculature, increases contractility and peripheral vasodilation
what is the dosing of milrinone?
bolus (optional): 50mcg/kg/IV over 10 min
infusion (0.25-0.75 mcg/kg/min)
renal adjustment: 0.2-0.43 mcg/kg/min based on CrCl
what are the ADRs of milrinone?
hypotension
ventricular arrhyth
HA
thrombocytopenia
reflex tachycardia
what is the MOA of levosimendan? what are its ADRs?
doesn't matter, not approved for use in the US; but just for fun:
calcium sensitizing agent in myocardium, some PDE3 inhibition - increase contractility and periph vasodilation
ADRs: hypotension, HA, tachycardia
match the following:
vasopressin decrease SVR
B2 increase CO and HR
a1 decrease UO
B1 increase SVR and MAP
vasopressin = decrease UO
B2 = decrease SVR
a1 = increase SVR and MAP
B1 = increase CO and HR