Lecture 3-Positive Inotropes Flashcards
Positive inotropes improve ___
The strength of contraction—they improve the squeeze out of the LV to get blood out into the body
___ is peripheral circulatory failure that results in underperfusion of tissues
Shock
Shock results in ___ (increased/decreased) oxygen delivery to tissues; ___ (increase/decrease) in anaerobic metabolism; more ___ (acidic/alkalotic) pH; ___ (increased/decreased) lactate
Shock results in decreased O2 delivery to tissues; increase in anaerobic metabolism; more acidic pH; increased lactate
Shock is a low cardiac output state—T/F?
True
3 types of shock =
- Septic
- Hypovolemic
- Cardiogenic
Septic shock = ___ (increased/decreased) CI; ___ (increased/decreased) PCWP; ___ (increased/decreased) SVR
Increased CI; decreased PCWP; decreased SVR
Hypovolemic shock = ___ (increased/decreased) CI; ___ (increased/decreased) PCWP; ___ (increased/decreased) SVR
Decreased CI; decreased PCWP; increased SVR
Cardiogenic shock = ___ (increased/decreased) CI; ___ (increased/decreased) PCWP; ___ (increased/decreased) SVR
Decreased CI; increased PCWP; increased SVR
In CHF, there is ___ (increased/decreased) intracellular cAMP
Decreased intracellular cAMP
CHF responds to ___ reduction, ___ reduction, and improved ___
Preload reduction, afterload reduction, and improved contraction
Low cardiac output syndrome (LCOS) can occur in patients coming off of CPB—T/F?
True
LCOS results in inadequate ___ delivery to tissues; hemo___; mild ___calcemia; ___magnesemia; ___uresis; tissue ___ gradients; variable levels of ___
Inadequate oxygen delivery to tissues; hemodilution; mild hypocalcemia; hypomagnesemia; kaliuresis (elimination of potassium through the kidneys); tissue thermal gradients; variable levels of systemic vascular resistance
Risk factors for LCOS—___; increasing age above ___; ___ (male or female?); pre-op decreased ___; increased duration of CPB (> ___ hours quickly increases the risk)
Diabetes; increasing age above 65; female; pre-op decreased LVEF; increased duration of CPB (> 6 hours quickly increases the risk)
LCOS is caused by a stunned myocardium—___contractile myocardium in response to ___ and ___
hypocontractile myocardium in response to ischemia and reperfusion
Beta receptor down regulation has been reported with LCOS—T/F?
True, but this takes weeks to occur
Treatment of LCOS = ___ (what drug class?)
Positive inotropes to increase the contractility of normal and stunned myocardium
Hypotension in LCOS responds well to vasodilators alone—T/F?
False—hypotension in LCOS (UNLIKE CHF) responds POORLY to vasodilators alone
In CHF, you can use vasodilators to reduce preload/afterload and reduce the workload on the heart—this helps to improve the strength of contraction/helps with hypotension
Goal of LCOS treatment in critically ill patients is to increase levels of O2 ___ (keep SvO2 > ___%) and increase O2 ___ (arterial blood lactate level < or equal to ___ mmol/L)
Increase levels of O2 delivery (keep SvO2 > 70%) and increase O2 consumption (arterial blood lactate level < or equal to 2 mmol/L)
(2) classes of positive inotropes:
- cAMP dependent
- cAMP independent
(3) cAMP dependent positive inotropes:
- Beta agonists
- Dopaminergic agonists
- Phosphodiesterase inhibitors
(2) cAMP independent inotropes:
- Cardiac glycosides
- Calcium
Hemodynamic effects of positive inotropes—___ (increased/decreased) contractility with ___ (increased/decreased) SV and often ___ (increased/decreased) LVEDP and volume
Increased contractility with increased SV and often decreased LVEDP and volume
Have reduced LV pressure/volume because you are pumping more blood out
“Pure” beta-1 agonists AKA inodilators = ___ and ___
Dobutamine and isoproterenol
Hemodynamic effects of “pure” beta-1 agonists/inodilators—___ (increased/decreased) HR; ___ (increased/decreased) AV conduction; ___ (increased/decreased) SVR and PVR; variable effect on myocardial ___
Increased HR; increased AV conduction; decreased SVR and PVR (beta 2 effect causing peripheral vasodilation in skeletal muscle/periphery); variable effect on myocardial O2 consumption
Mixed alpha/beta agonists AKA inoconstrictors = ___, ___, and ___
Norepi, epi, and dopamine
Hemodynamic effects of mixed alpha/beta agonists AKA inoconstrictors—___ (increased/decreased) vascular resistance; ___ (increased/decreased) myocardial O2 consumption; ___ (increased/decreased) HR
Increased vascular resistance; increased myocardial O2 consumption; increased HR
If you have both a reduction in cardiac output and SVR, it would be best to use an inodilator like dobutamine or isoproterenol—T/F?
False—it would be best to use an inoconstrictor like norepi, epi, or dopamine
Contraindications/complications of positive inotropes—isoproterenol, dobutamine, and dopamine may worsen ___
Tachyarrhythmias
Contraindications/complications of positive inotropes—high doses of NE and epi for prolonged periods with persistent low CO will ___ (increase/decrease) perfusion to many tissue beds and contribute to ___ failure
Decrease perfusion to many tissue beds and contribute to renal failure
Contraindications/complications of positive inotropes—digoxin should be used cautiously in patients with ___kalemia, ___ failure, ___cardia, and drug ___
Hypokalemia, renal failure, bradycardia, and drug interactions
Goal with positive inotropes is to use the lowest dose possible for the shortest period of time possible—T/F?
True
Arrhythmogenic potential of positive inotropes (in order of least to greatest risk):
Dobutamine < dopamine < epi < isoproterenol
Which positive inotrope has the greatest arrhythmogenic potential?
Isoproterenol
Norepi has high risk of arrhythmias—T/F?
False—norepi improves CO/SV but does not come with significant increases in HR, so it has less arrhythmogenic potential
CAMP dependent positive inotropes MOA—catecholamines bind to beta receptors and activate a membrane-bound guanine nucleotide binding protein; this activates ___ and generates ___; ___ increases ___ influx via slow channels and increases sensitivity of regulatory proteins; result is ___ (increased/decreased) force of contraction and velocity of relaxation through the movement of ___ (what electrolyte?)
This activates adenylyl cyclase and generates cAMP; cAMP increases Ca influx via slow channels and increases sensitivity of regulatory proteins; result is increased force of contraction and velocity of relaxation through the movement of Ca
Review—epi stimulates ___, ___, and ___ receptors
Alpha 1, beta 1, and beta 2 receptors
Low dose epi = primarily ___ effects in the ___
Primarily beta 2 effects in the peripheral vasculature
Low dose epi—the net effect is ___ (increased/decreased) SVR and distribution of blood to ___; MAP essentially remains ___
The net effect is decreased SVR and distribution of blood to skeletal muscle; MAP essentially remains the same
Low dose epi is essentially a vaso___
Vasodilator
Intermediate dose epi = ___ effects; increased ___, ___, and ___
Inotropic/beta 1 effects; increased HR, contractility, and CO
High dose epi > 10 mcg/min = ___ effects; potent vaso___; used to maintain ___ and ___ perfusion; reflex ___cardia can occur
Alpha 1 effects; potent vasoconstrictor; used to maintain myocardial and cerebral perfusion; reflex bradycardia can occur
Norepi is primarily an ___ agonist
Alpha 1 agonist
Norepi—cardiac output may ___ (increase/decrease) at low doses, but at higher doses may ___ (increase/decrease) because of ___ and ___
Cardiac output may increase at low doses, but at higher doses may decrease because of increased afterload and baroreceptor-mediated reflex bradycardia
What is the vasoconstrictor of choice for septic shock?
Norepi—maintains peripheral vasculature/improves cardiac output
Isoproterenol has ___ and ___ receptor effects
Beta 1 and beta 2 receptor effects…beta all day
Isoproterenol increases ___, ___, and ___
Heart rate, contractility, and cardiac automaticity
Positive chronotrope, inotrope, and dromotrope
Isoproterenol ___ (increases/decreases) SVR and diastolic BP because of negative feedback
Decreases SVR and diastolic BP because of negative feedback
When you increase the workload on the heart like isoproterenol does, then the vasculature will relax in response to that
Isoproterenol is an ino___
Dilator
Net effect of isoproterenol is ___ (increased/decreased) cardiac output and ___ (increased/decreased) MAP
Increased cardiac output and decreased MAP
Side effects of isoproterenol—___cardia; diastolic ___tension; ___ (increased/decreased) myocardial oxygen consumption; ___ (increased/decreased) incidence of cardiac dysrhythmias
Tachycardia; diastolic hypotension; increased myocardial oxygen consumption; increased incidence of cardiac dysrhythmias
Isoproterenol should be avoided in patients in ___ or in patients with ___
Avoided in patients in cardiogenic shock or in patients with ischemic heart disease
Uses of isoproterenol—chemical pacemaker after ___ or in ___; broncho___ management during anesthesia; decrease ___ in patients with pulmonary HTN/RV failure
Chemical pacemaker after heart transplant or in complete heart block; bronchospasm management during anesthesia; decrease PVR in patients with pulmonary HTN/RV failure
Dobutamine is a synthetic catecholamine with structural characteristics of ___ and ___
Dopamine and isoproterenol
Dobutamine acts primarily on ___ receptors
Beta 1 receptors (with small effects on beta 2 and alpha 1 receptors)
Dobutamine has no clinically significant vaso___ activity; ___ (more/less) increase in conduction compared to isoproterenol; less likelihood of adverse increase in myocardial ___ requirements; dilates ___ vasculature; no ___ receptor activation
No clinically significant vasoconstrictor activity; less increase in conduction compared to isoproterenol; less likelihood of adverse increase in myocardial O2 requirements; dilates coronary vasculature; no dopaminergic receptor activation
Dobutamine may NOT be effective in patients who need increased ___ to increase ___
Increased SVR to increase BP (because it is an inodilator and only improves cardiac output)
What should you use for a patient who needs increased SVR/BP?
Inoconstrictor (norepi, epi, dopamine)
Dobutamine must be prepared in ___ solution
D5W
Dobutamine can be inactivated if prepared in ___ IV solutions
Alkaline IV solutions (i.e.: NS)
Two types of dopaminergic agonists:
- D1 like
- D2 like
D1 like dopaminergic agonists ___ (stimulate/inhibit) adenylate cyclase and ___ (activate/inhibit) cAMP; results in smooth muscle vaso___
Stimulate adenylate cyclase and activate cAMP; results in smooth muscle vasodilation
D2 like dopaminergic agonists ___ (stimulate/inhibit) adenylate cyclase and ___ (activate/inhibit) cAMP; promotes vaso___
Inhibit adenylate cyclase and inhibit cAMP; promotes vasodilation
D1 like dopaminergic agonists ___ (increase/decrease) gastric secretion/acidity; D2 like dopaminergic agonists ___ (increase/decrease) gastric secretion/acidity
D1 decreases, D2 increases gastric secretion/acidity
Both D1 and D2 dopaminergic agonists ___ (stimulate/inhibit) aldosterone secretion from the adrenal glands
Inhibit
Low dose (renal dose) dopamine may increase RBF, GFR, Na+ excretion and urine output but is NOT renal protective—T/F?
True
Low dose (renal dose) dopamine is not predictable; tolerance to renal effects develops after 2-48 hours; and there has been no benefit of renal dose dopamine for the prevention/treatment of renal failure—T/F?
True
Intermediate dose dopamine has ___ receptor effects—results in ___ (increased/decreased) myocardial contractility/CO without marked changes in ___ or ___
Beta receptor effects—results in increased myocardial contractility/CO without marked changes in HR or BP
Part of the beta effects of intermediate dose dopamine is due to the release of endogenous stores of ___, which predisposes patients to cardiac ___
Release of endogenous stores of NE, which predisposes patients to cardiac dysrhythmias
Dopamine may be used in clinical situations where the patient presents with decreased ___, decreased systemic ___, or increased ___
Decreased CO, decreased systemic BP, or increased LVEDP
Dopamine interferes with the ventilatory response to ___ through its inhibitory role at the ___
Interferes with the ventilatory response to hypoxemia through its inhibitory role at the carotid bodies
High doses of dopamine inhibit the release of ___, causing ___
Inhibit the release of insulin, causing hyperglycemia
Dopamine must be prepared in ___
D5W (just like dobutamine)
Side effects of dopamine—___/___; ___cardia; ___ pain d/t increased myocardial oxygen consumption; ___ (less than isoproterenol, higher risk than dobutamine); ___ache; ___tension; peripheral vaso___
Nausea/vomiting; tachycardia; angina pain d/t increased myocardial oxygen consumption; arrhythmias (less than isoproterenol, higher risk than dobutamine); headache; hypertension; peripheral vasoconstriction
Dopamine can cause nausea/vomiting through its ___ receptor activation
D2 receptor activation
Fenoldopam (corlopam) is a selective ___ agonist with moderate affinity for presynaptic ___ receptors
Selective D1 agonist with moderate affinity for presynpatic alpha 2 receptors
Fenoldopam (corlopam) ___ (increases/decreases) SVR and renal vasculature resistance, resulting in ___ (increased/decreased) BP and ___ (increased/decreased) LVEF and RBF
Decreases SVR and renal vasculature resistance, resulting in decreased BP and increased LVEF and RBF
What can occur if fenoldopam (corlopam) is titrated up too quickly?
Reflex tachycardia
Fenoldopam (corlopam) is a last resort medication to treat severe ___
Hypertension
Fenoldopam (corlopam) can be titrated quickly—T/F?
False—needs to be titrated very slowly otherwise you may have a lot of complications with BP/HR
Fenoldopam (corlopam) can be given as a bolus—T/F?
False—do NOT bolus
Fenoldopam (corlopam) preserves RBF, UO, and is renal protective—T/F?
False-ish—it does preserve RBF and UO, but it is NOT renal protective
With slow titration of fenoldopam (corlopam), there is no increase in HR or arrhythmias—T/F?
True
Side effects of fenoldopam (corlopam) include ___ache, ___ syndrome, sweating/flushing, nausea, ___ wave inversion, dizziness, and slight increase in ___
Headache, restless leg syndrome, sweating/flushing, nausea, T wave inversion, dizziness, and slight increase in IOP
Hemodynamics summary—phenylephrine ___ (increases/decreases) PWP; ___ (increases/decreases/has no effect) on CO; ___ (increases/decreases) SVR; ___ (increases/decreases) MAP
Increases PWP; has no effect on CO; increases SVR; increases MAP
Hemodynamics summary—norepinephrine ___ (increases/decreases) PWP; ___ (increases/decreases/has no effect) on CO; ___ (increases/decreases) SVR; ___ (increases/decreases) MAP
Increases PWP; has no effect on CO; increases SVR; increases MAP
Hemodynamics summary—epinephrine ___ (increases/decreases) PWP; ___ (increases/decreases) CO; ___ (increases/decreases) SVR; ___ (increases/decreases) MAP
Decreases or increases PWP; increases CO; decreases or increases SVR; increases MAP
Hemodynamics summary—dopamine ___ (increases/decreases) PWP; ___ (increases/decreases) CO; ___ (increases/decreases) SVR; ___ (increases/decreases) MAP
Increases PWP; increases CO; increases SVR; increases MAP
Hemodynamics summary—dobutamine ___ (increases/decreases) PWP; ___ (increases/decreases) CO; ___ (increases/decreases) SVR; ___ (increases/decreases/has no effect) MAP
Decreases PWP; increases CO; decreases SVR; has no effect on MAP
Hemodynamics summary—isoproterenol ___ (increases/decreases) PWP; ___ (increases/decreases) CO; ___ (increases/decreases) SVR; ___ (increases/decreases/has no effect) MAP
Decreases PWP; increases CO; decreases SVR; has no effect on MAP
Phosphodiesterase breaks down ___, which stops the action of bringing ___ into the cell
Cyclic AMP, which stops the action of bringing calcium into the cell
Phosphodiesterase inhibitors increase ___, resulting in continued ___ effects
Increase cAMP, resulting in continued calcium effects
CAMP dependent positive inotropes are AKA phosphodiesterase ___ inhibitors
Phosphodiesterase 3 inhibitors
Phosphodiesterase 3 inhibitors increase intracellular ___ concentrations; increase the ___ sensitivity of contractile proteins; increase ___ influx; peripherally, cause arterial and venous vaso___; results in increased ___
Increase intracellular cAMP concentrations; increase the Ca sensitivity of contractile proteins; increase Ca influx; peripherally, cause arterial and venous vasodilation; results in increased CO
Inamrinone causes dose-dependent increases in ___ and ___ and decreases in ___ and ___ after CABG
Increases in SV and CI and decreases in SVR and PVR after CABG
Inamrinone has proven to be more effective with fewer complications than dobutamine during separation from CPB—T/F?
True
In patients with poor LV function, inamrinone is as effective as epi, but inamrinone and epi are superior to either drug alone—T/F?
True
Adverse reactions/cautions with inamrinone—can cause ___ in 10% of patients; elevated ___; ___; do NOT administer to patients with ___; may aggravate outlet obstruction in patients with ___
Can cause thrombocytopenia in 10% of patients; elevated LFTs; arrhythmias; do NOT administer to patients with aortic stenosis (results in bad outcomes); may aggravate outlet obstruction in patients with idiopathic hypertrophic subaortic stenosis (IHSS)
If patient has platelet count < 150K and is on inamrinone, how should you adjust the inamrinone dose?
Reduce inamrinone dose
Milrinone (primacor) has inotropic and vasodilator properties similar to inamrinone, but it is ___-___ times more potent with a shorter half-life (___ hours) and without the risk of ___
15-20 times more potent with a shorter half-life (2.5 hours, so it would be completely out of someone’s system in ~12 hours) and without the risk of thrombocytopenia
Loading dose of milrinone (primacor) is not really recommended if you are using it for a longer duration/going to be putting the patient on a milrinone infusion—T/F?
True
Can use loading dose of milrinone when separating the patient from CPB
Milrinone side effects—___ache, ___tension, ___ope; ventricular ___ (~___%); increased ventricular response rate in ___ and ___
Headache, hypotension, syncope; ventricular arrhythmias (~10%); increased ventricular response rate in A-fib and A-flutter
Glucagon acts at ___ receptor on the myocardium to increase ___
Glucagon receptor on the myocardium to increase cAMP
Glucagon ___ (increases/decreases) CI, HR, BP and ___ (increases/decreases) SVR and LVEDP
Increases CI, HR, BP and decreases SVR and LVEDP
Glucagon is useful in cardiac failure precipitated by ___
Beta blockade
Glucagon use is limited due to side effects—___/___; increased ___; increased ___ and ___ vascular resistance
Nausea/vomiting; increase blood sugar; increase coronary and pulmonary vascular resistance
Glucagon can be used to treat ___ and ___ toxicity
Beta blocker and CCB toxicity
Glucagon drug interactions—___ medications enhance glucagon GI side effects (nausea/vomiting); ___ increase INR
Anticholinergic medications enhance glucagon GI side effects (nausea/vomiting); vitamin K antagonists (i.e.: warfarin) increase INR
Digoxin is a ___
Cardiac glycoside
Digoxin is a positive ___, negative ___, and negative ___
Positive inotrope (increases strength of contraction), negative dromotrope (decreases speed of conduction through AV node), and negative chronotrope (decreases HR)
How does digoxin work? It inhibits ___; the reduced ___ gradient slows ___ removal
It inhibits Na+/K+ ATPase (3 Na+ out for 2 K+ in); the reduced Na gradient slows Ca removal (so more Ca stays inside the cardiac myocyte to improve contractility)
Use of digoxin—positive inotrope for treatment of mild to moderate ___ (often used in combo with a ___ and ___); control of ventricular response rate in patients with chronic ___
Positive inotrope for treatment of mild to moderate heart failure (often used in combo with a diuretic and ACE inhibitor); control of ventricular response rate in patients with chronic AFib
No clinical trials have demonstrated that digoxin improves mortality for patients with CHF—T/F?
True
Patients with CHF on digoxin may experience less hospitalizations—T/F?
True
Beta blockers/CCBs are much more effective at reducing heart rate than digoxin—T/F?
True
Digoxin has a very narrow therapeutic range—___-___ ng/mL
0.8-2 ng/mL
Digoxin toxicity can occur at plasma levels > ___ ng/mL
> 3 ng/mL
Digoxin toxicity is associated with a decrease in intracellular ___
Potassium (because it is blocking the Na+/K+ ATPase pump)
Predisposing causes of digoxin toxicity—___kalemia; ___magnesemia; ___emia; ___calcemia; ___thyroid
Hypokalemia; hypomagnesemia; hypoxemia; hypercalcemia; hypothyroid
Digoxin toxicity presentation—early signs = ___, ___/___
Anorexia, nausea/vomiting
What is the most common dysrhythmia associated with digoxin toxicity?
Paroxysmal atrial tachycardia with block
What is the most frequent cause of death from digoxin toxicity?
VFib
Treatment of dig toxicity—correct ___ causes; administer drugs—___ or ___ to suppress ventricular dysrhythmias; ___ to increase HR; ___ to suppress increased automaticity; temporary ___ if complete heart block is present
Correct predisposing causes (i.e.: electrolyte imbalances, hypoxemia); administer drugs—phenytoin or lidocaine to suppress ventricular dysrhythmias; atropine to increase HR; beta blocker to suppress increased automaticity; temporary pacing if complete heart block is present
What is the antidote for digoxin?
Digibind
How does digibind work?—___ bind to the drug and decrease plasma concentrations of cardiac glycosides
Fab (antibody fragments) bind to the drug
Fab-digitalis complex is eliminated by the ___
Kidneys
You should check digoxin levels shortly after administering digibind?—T/F?
False—do not check levels for several days
Patients with kidney failure will take several days to remove the digoxin/digibind complex from the body; if you check levels too early, you will still see high levels of digoxin because it hasn’t been removed from the body yet.
When bound to digibind, digoxin is still active until the whole complex is removed by the kidneys—T/F?
False—digoxin becomes inactive when bound up by digibind
Digoxin drug interactions—quinidine, amiodarone, verapamil, propafenone, coreg, cyclosporine, and conivaptan ___ (increase/decrease) clearance of digoxin
DECREASE clearance of digoxin (so would increase your risk of digoxin toxicity)
Digoxin drug interactions—macrolides, PPIs, conazoles, ranolazine ___ (enhance/decrease) digoxin absorption
Enhance
Digoxin drug interactions—resin binders, acarbose/miglitol, kaolin-pectins, reglan, sulfasalazine, and sucralfate ___ (enhance/decrease) digoxin absorption
Decrease
Therapeutic plan for low cardiac output—goal is to optimize heart ___ and ___
Optimize heart rate and rhythm
Therapeutic plan for low CO—first thing you want to do is optimize ___
Preload
Increase intravascular volume as long as these additions increase SV and don’t produce excessive increases in ventricular filling pressures that lead to pulmonary edema or myocardial ischemia
Therapeutic plan for low CO—what medication class should you use to optimize preload?
Venous vasodilators (i.e.: nitroglycerine)
Therapeutic plan for low CO—if BP is acceptable after increasing preload, administer an ___ dilator to increase SV (optimize ___); if further support is needed, add an ___; alternatively, can add an ino___
Administer an arteriolar dilator to increase SV (optimize afterload); if further support is needed, add an inotrope; alternatively, can add an inodilator (i.e.: inamrinone, milrinone, dobutamine)
Therapeutic plan for low CO—for low BP, add an ___; once BP is acceptable, if SV is still depressed, add an ___ vasodilator; if SVR is low, add an ___
Inotrope; once BP is acceptable, if SV is still depressed, add an arteriolar vasodilator; if SVR is low, add an inoconstrictor (i.e.: norepi, epi, dopamine)
Positive inotropes—initial drug selection—if patient has pulmonary and/or systemic HTN, use ___, ___ or ___, ___
Dobutamine, inamrinone or milrinone, or isoproterenol
Positive inotropes—initial drug selection—if low SVR, use ___
Inoconstrictor—norepi, epi, dopamine
Positive inotropes—initial drug selection—if normal PVR and SVR, can use ___ or ___
Dopamine or epi
Positive inotropes—initial drug selection—if tachycardic, can use ___ or ___, ___, ___, ___
Can use inamrinone or milrinone, calcium, norepi, epi (epi is not really best choice for patient who is already tachycardic)
Persistent low CO or myocardial ischemia with maximal medical therapy indicates the need for ___ or ___
IABP or LVAD
ALARM-HF Trial—found there was ___ (lower/higher) mortality for patients receiving vasodilator + diuretic vs. diuretic alone
Lower mortality
7.6% mortality for vasodilator+diuretic vs. 14.2% mortality for diuretic alone
ALARM-HF Trial—found there was ___ (lower/higher) mortality for IV inotropes vs. no inotropes
Higher mortality for IV inotropes vs. no inotropes
25.9% mortality for IV inotropes vs. 5.2% mortality for no inotropes
ALARM-HF Trial—found there was a ___ fold increase in mortality for patients receiving dopamine or dobutamine; ___ fold increase in mortality for patients receiving NE or epi
1.5 fold increase in mortality for patients receiving dopamine or dobutamine; 2.5 fold increase in mortality for patients receiving NE or epi
___ are great for HF patients
Vasodilators
Inotropes increase mortality for HF patients—T/F?
True
If patient has high pressures (PAOP/MAP), use a ___ to improve ___; can also remove fluid with a ___ to decrease high pressures
Use a venous vasodilator (i.e.: NTG) to improve preload; can also remove fluid with a diuretic to decrease high pressures
If patient has low pressures (PAOP/MAP), use ___ if HR is normal; if HR is low, use ___ or ___
Use norepi if HR is normal; if HR is low, use dopamine or epi
