hemodynamic monitoring 2
Terms
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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?
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1. to measure cardiovascular performance
2. to assess etiology of shock states (hypoperfusion and organ dysfunction) - 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 - 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?
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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 - 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 - what three factors affect stroke volume?
- preload, afterload, contractility
- 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) - what is afterload? how is it estimated?
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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?
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CI: normalization of CO to body size
CI = CO/BSA - 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 - 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 - 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?
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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?
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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) - 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
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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 -
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
- 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) - 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 - what are the advantages of using crystalloids?
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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?
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very expensive
may not be readily available - 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) - 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?
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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) - 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 - 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 - what is the physiologic and hemodynamic effect of stimulating B2 receptors?
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physiologic: arterial and venous vasodilation
hemodynamic: decrease in SVR - what is the physiologic and hemodynamic effect of stimulating DA receptors?
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physiologic: vasodilation
hemodynamic: ? increase in UO? - 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 - 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 - Dopamine works on which receptors?
- DA, B1, a1
- 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? - 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 - 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 - 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?
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tachyarrhythmia
increased afterload and preload
increased myocardial oxygen demand (can cause MI)
peripheral ischemia
pulmonary congestion - Norepinephrine stimulates which receptors and causes what effects?
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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?
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increased afterload
cardiac arrhythmias
peripheral ischemia
increased myocardial oxygen demand (not as much as DA) - 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) - 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?
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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?
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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) - 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 - what are the ADRs associated w/ epi?
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increased in myocardial ox demans
tachyarrhythmias
ischemia
lactic acidosis - 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 - 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?
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decrease CO
myocardial and splanchnic ischemia (necrotic bowel) - 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) - 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?
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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?
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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 - what are the ADRs of milrinone?
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hypotension
ventricular arrhyth
HA
thrombocytopenia
reflex tachycardia - 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 -
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