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80 Cards in this Set
- Front
- Back
what is the definition of hemodynamic monitoring?
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the study of physical factors regulating blood flow
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what is the purpose of hemodynamic monitoring?
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1. to measure cardiovascular performance
2. to assess etiology of shock states (hypoperfusion and organ dysfunction) |
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what are the five hemodynamic components?
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BP - blood pressure
MAP - mean arterial pressure CO - cardiac output CI - cardiac index SVR - systemic vascular resistance |
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How is MAP calculated?
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2/3 diastolic BP + 1/3 systolic BP = MAP
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Blood pressure: what is it, what is it associated with, how is it calculated?
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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 |
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Cardiac output: what is it and how is it calculated?
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CO is the volume of blood ejected per minute (L/min)
CO = SV x HR |
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what three factors affect stroke volume?
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preload, afterload, contractility
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what is preload? how is it estimated?
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preload: how much blood is going to the left ventricle
LVEDV is estimated by the PCWP (the volume right before systole) |
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what is afterload? how is it estimated?
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afterload: resistance of the left ventricle
it is estimated by SVR |
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what is the term used to describe contractility?
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inotropy
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what is cardiac index and how is it calculated?
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CI: normalization of CO to body size
CI = CO/BSA |
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what are some non-invasive measures of hemodynamics? (3)
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vital signs (BP, HR)
pulse oximetry (PaO2) transthoracic echocardiogram (TTE) - measures ejection fraction |
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what are some invasive measures of hemodynamics? (3)
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arterial line (PaO2)
central venous catheter (meaures BP - fluid status of the venous side) pulmonary arterial catheter |
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describe the frank starling mechanism
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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
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what is a pulmonary arterial catheter useful for?
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volume status
ventricular performance estimating Oxygen delivery and uptake can help differentiate between shock syndromes |
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true or false: use of a PAC will decrease mortality
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false: use of a PAC will cause no difference in mortality
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what are some potential adverse effects of using a PAC?
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it can lead to premature atrial or ventricular contractions and pulmonary artery rupture
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which direct measurements and calculated measurements can a PAC be used to obtain?
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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) |
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what is the normal value for CO?
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4-7 L/min
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what is the normal range for CI?
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2.8-4.5 L/min/m2
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what is the normal range for SV?
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60-100mL
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what is the normal range for SVR?
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900-1400 dynes*sec/cm5
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what is the normal range for PCWP?
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6-15 mmHg
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what is the normal range for CVP?
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2-6 mmHg
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what is the normal range for MAP?
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80-100 mmHg
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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 |
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assess the following clinical situation:
pts CI is 1.5 and PCWP is 10 |
hypovolemic shock
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assess the following clinical situation:
pts CI is 1.5 and PCWP is 23 |
cardiogenic shock
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assess the following clinical situation:
pts CI is 3 and PCWP is 12 |
normal
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assess the following clinical situation:
pts CI is 3 and PCWP is 25 |
pulmonary edema
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what are the goals of pharmacologic therapy in managing hemodynamic instability?
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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) |
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what are the categories of fluids and what are some examples of each?
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crystalloids: Normal saline (NS) and lactated ringers (LR)
colloids: albumin 5% and hetastarch 6% blood |
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what are the advantages of using crystalloids?
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low cost
widely available |
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what is one advantage to using lactated ringers?
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the bicarbonate is good for pts w/ acidosis
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what is a disadvantage to using crystalloids?
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only 25-33% remain in intravascular space
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when giving fluids, what compartment do we want it to stay in?
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intravascular - plasma
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what is an advantage to using colloids?
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80-100% remain in intravascular space
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what are some disadvantages to using colloids?
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very expensive
may not be readily available |
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what types of blood products are used in treating hemodynamic instability?
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whole blood
packed red blood cells (PRBC) platelets crypoprecipitate (clotting factors) |
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when is the use of blood products indicated in pts w/ hemodynamic instability?
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only if Hgb is decreased or if there is a loss of blood
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what are the treatment goals when administering fluids to a hemodynamically unstable pt?
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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) |
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what is the physiologic and hemodynamic effect of stimulating a1 receptors?
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physiologic: arterial and venous vasoconstiction
hemodynamic: increase in SVR and MAP |
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what is the physiologic and hemodynamic effect of stimulating B1 receptors?
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physiologic: increase in contractility and chronotropy
hemodynamic: increase in CO and HR |
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what is the physiologic and hemodynamic effect of stimulating B2 receptors?
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physiologic: arterial and venous vasodilation
hemodynamic: decrease in SVR |
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what is the physiologic and hemodynamic effect of stimulating DA receptors?
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physiologic: vasodilation
hemodynamic: ? increase in UO? |
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what is the physiologic and hemodynamic effect of stimulating VP receptors?
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physiologic: vasoconstriction, fluid retention, increase in cortisol
hemodynamic: increase in SVR and MAP |
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classify the following agents as either vasopressors (increase SVR) or inotropes (increase in CO): dopamine, dobutamine, vasopressin, norepinephrine, milrinone, levosimendan, epinephrine, phenylephrine
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vasopressors: dopamine, norepinephrine, epinephrine, phenylephrine, vasopressin
inotropes: dopamine, dobutamine, milrinone, levosimendan |
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Dopamine works on which receptors?
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DA, B1, a1
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what dose of dopamine is used for stimulating DA receptors and what is the effect?
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0.5-3 mcg/kg/min
increases renal and mesenteric blood flow, mesenteric/renal/cerebral/coronary arterial dilatation, ? increase in UO? |
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what dose of dopamine is used for stimulating B1 receptors and what is the effect?
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3-10 mcg/kg/min
increase inotropy (contractility) and chronotropy (HR), increase CO |
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what dose of dopamine is used for stimulating a1 receptors and what is the effect?
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10-20 mcg/kg/min
incease in peripheral vasoconstriction, SVR, MAP |
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what effect dose dopamine have on renal tubules?
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inhibits proximal tubule sodium reabsorption
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Dopamine stimulates the release of ______________?
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norepinephrine
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true or false: renal dose dopamine decreases mortality of critically ill pts by preventing acute renal failure
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false: renal dose dopamine should never be used
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what adrs are associated with dopamine?
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tachyarrhythmia
increased afterload and preload increased myocardial oxygen demand (can cause MI) peripheral ischemia pulmonary congestion |
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Norepinephrine stimulates which receptors and causes what effects?
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a1 receptors: increase peripheral vasoconstriction (increase SVR)
negligible B effects |
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what effect does pH have on NE? why is this important?
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decreased activity in acidosis, may need to increase dose; if organs are not perfused, may lead to anaerobic metabolism - leads to acidosis
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what is the normal dosing range of NE?
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2-50 mcg/min (max 200); dose titrated to MAP > 65 mmHg
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what ADRs are associated w/ NE?
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increased afterload
cardiac arrhythmias peripheral ischemia increased myocardial oxygen demand (not as much as DA) |
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phenylephrine stimulates which receptors and causes what effects?
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stimulation of a1 receptors: increase in peripheral vasoconstriction
no B effects (no increase in myocardial oxygen demand) |
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what is the normal dosing range of phenylehprine?
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30-300 mcg/min (max 200) titrated to MAP >65 mmHg
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what ADRs are associated w/ phenylephrine?
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increased afterload
reflex bradycardia peripheral bradycardia peripheral ischemia*** myocardial ischemia hypertension |
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why is phenylephrine considered second line?
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extreme peripheral ischemia - may lead to amputation
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why should pressors be d/c's ASAP?
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they can cause peripheral ischemia
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epinephrine works on which receptors and causes what effects?
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stimulation of a1 receptors: increase peripheral vasoconstriction
stimulation of B receptors: increase in inotropy/chronotropy, increase in peripheral vasodilation (effects are dose dependent) |
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what are the normal doses for epinephrine?
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B1, B2: 0.01-0.05 mcg/kg/min - increase in SVR/MAP
a1, B1: >0.05 - increase in CO, HR, contractility |
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what are the ADRs associated w/ epi?
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increased in myocardial ox demans
tachyarrhythmias ischemia lactic acidosis |
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what receptors does vasopressin stimulate? what are the effects of each?
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VP1: peripheral vasoconstriction
VP2: sodium and water retention, decreased UO **VP3: increase ACTH and cortisol production |
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when is vasopressin used and what is the benefit?
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used in adjunct to other pressors in septic shock. benefit= you can decrease the dose of other pressors when you add vasopressin
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what is the normal dosing of vasopressin?
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0.01-0.04 units/min
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what are the ADRs associated w/ vasopressin?
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decrease CO
myocardial and splanchnic ischemia (necrotic bowel) |
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what receptor does dobutamine stimulate? what is the effects?
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B receptor: increase inotropy/chronotropy, increase CO
a1 receptor: minimal - increase in peripheral vasoconstriction (smaller effect than B1 effects) |
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what is the normal dosing of dobutamine?
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2.5 mcg/kg/min (max 20 mcg/kg/min) titrate to desired CI
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what are the ADRs associated w/ dobutamine?
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ventricular arrhythmia
hypotension (usually does cause this) increase myocardial O2 demand |
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when is dobutamine C/I?
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SBP < 100mmHg
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what is the moa if milrinone? what is its effects?
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MOA: PDE-3 inhibitor - inhibits breakdown of cAMP in myocardium and vasculature, increases contractility and peripheral vasodilation
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what is the dosing of milrinone?
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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 |
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what are the ADRs of milrinone?
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hypotension
ventricular arrhyth HA thrombocytopenia reflex tachycardia |
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what is the MOA of levosimendan? what are its ADRs?
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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 |
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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 |