Heart Failure



Progressive Disease: any structural or functional impairment of:
o Ventricular filling (diastolic dysfunction) – small pool
o Ejection of blood (systolic dysfunction) – no strength to pump out
HF= Chronic HF (CHF), but NOT: cardiomyopathy or left ventricular dysfunction
o Black males – highest risk HF
o Mortality rate: 50% w/in 5 years of diagnosis
Normal Heart Anatomy
o Left: Left atriumMitral valveLeft VentricleAortic valveBody
 Back into heart via lungs to push out to the body.
 Systolic HF: weak LV, blood pools and wont pump out.
 Diastolic HF: thick stiff muscle, wont fill up.
o Right: Right atriumTricuspidRight VentriclePulmonary valveLungs
 Preparing blood to leave heart.
Risk Factors

Modifiable: Smoking, Diet/Obesity, Immobility, Alcohol

Common Causes
Dilated Cardiomyopathies
(ineffective pumping)


Ventricular dilation and
depressed myocardial
contractility
HTN or valvular diseases
Drugs
Compensatory Mechanisms
(impaired LV)
Non-Modifiable: Age, Heredity, Race (AA male), Comorbidities
-#1 HTN, DM, Arrhythmia, Virus, Cardiomyopathies, Myocarditis, IHD, Vascular/valvular
disease, CKD, Dyslipidemia, Cardiotoxic drugs, Systemic toxins, Metabolic Syndrome
-Others: Thyroid disease, Growth Hormone deficiency, Iron overload, Stress,
Tachycardia.
CAD & Ischemic Damage
Non-Ischemic
-1/3 of patients.
-2/3 of pts.
-Intrinsic myocardial disease: valvular disease, myocarditis,
-LV/systolic dysfunction
autoimmune.
of heart.
-Excess work load: resistance to ejection (HTN, aortic
-Ischemic damage has
stenosis).
affected pumping.
 SV (valvular disease) (aortic, mitral, tricuspid insuff.)
-CHD/MI present.
  demand (thyrotoxicosis, anemia, pregnancy etc.)
-Iatrogenic: drugs and radiation
 Na/H2O retention (NSAIDS, steroids)
 contractility (BB, CCB)
 BV (IV fluids, albumin)
 Activate RAAS: Na & fluid retention, SNS (A1-A2 conversion)

SNS: (+) feedback, RAAS stimulated, heart tries pumping fast

Remodeling and other cellular changes: damage electrical conduction (arrhythmia),
function of myocytes & amount of vasodilators (b/c +feedback), enlarged
ventricles (increase O2 demand & decrease O2 supply)


Cardinal Manifestations: dyspnea, fatigue, fluid retention
Left Heart Dysfunction
Right Heart Dysfunction
Symptoms: DOE or @rest, fatigue, orthopnea,
 Symptoms: swelling, anorexia, abdominal
PND, cough, mental, cool extremities. (Lungs,
bloating & pain. Caused by Left Dysf. (worse,
fluid built up)
body SE’s)
Signs: cardiomegaly, tachycardia, HTN, pulm
 Signs: cardiomegaly, edema, JVD, HJR,
edema & HTN, rales & crackles, RF, Cheynes
ascites, hepatomegaly, splenomegaly, loss of
Stokes (b/c fluid in lungs).
appetite.
SV: amount of blood ejected after contraction (Preload-Afterload=SV)
EF: SV + Preload(EDV), fraction ejected each heartbeat, pump efficiency.


ECHO: live view of heart motion, estimate EF (TTE’s & TEE’s)
Chest X-ray: show shape of heart, pulmonary congestion.


BNP: formed by cardiomyocytes with myocardial stretch. Over 400, can be falsely elevated.
CBC &CMP: look for anemia/infection, renal/liver function & electrolytes (dilutional Na due to
fluid overload).
Presentation


Diagnosis
Based on
symptoms, no true
diagnostic test
HFrEF


Systolic HF: EF  40%. Ejection problem (no strength)
Structural ventricular hypokinetic abnormalities
Lifestyle Mod.
Interventional
Tx.
HFpEF

 Diastolic HF: EF  50%. Filling problem (small pool)
 Diagnosis of exclusion
 Borderline HFpEF: EF 41-49%
Exercise:  symptoms, improve exercise capacity, slows progression (decondition)

Na Restrict: target -  1.5-2g daily,  fluid accumulation

Fluid Restrict: target -  1.5-2L daily


Record home BP, pulse & weight (sign of fluid).
Operation: CAD (CABG, PCI/stent), Valve repair. Options for stages B & C.

Implant Cardioverter Defibrillator (ICD): Stages B or C, deactivated in D.

Cardiac Resynch Therapy (CRT): Stage C

Mechanical Circulatory Support (MCS): VAD’s (help ventricles), Stage D, Class 2a recommendation,
bridge to recovery, prolong survival.

Cardiac Transplant: Stage D, Class 1 recommendation.
Classifications
ACCF/AHA Stages of HF




NYHA Functional Classification
(development & progression of disease)
(CANNOT move back in stage!)
A: high risk HF, no structural heart disease or symptoms.
o (ACE/ARB) (can statins)
B: Structural heart disease, no signs or symptoms.
o Operation, ICD (ACE/ARB, Entresto) (can BB’s)
C: Structural heart disease, prior or current symptoms.
o Operation, ICD, CRT (all meds)
D: Refractory HF, require specialized interventions.
o Deactivate ICD, MCS, Transplant (iontropes)




(exercise capacity & symptom status)
(CAN move back in classification!)
1: no activity limits, ordinary activity – no symptoms.
o A, B & C (same as 2) “exercise induced”
2: slight limit, comfy @rest, ordinary activity – symptoms.
o (all pt’s try to be on BB’s)
3: marked limit, comfy @rest,  ordinary – symptoms.
o C
4: no physical activity, symptoms @ rest.
o C&D
Goals of Therapy
Stage A



Stage C
Heart healthy lifestyle
Prevent vascular/coronary disease & LV structural
abnormalities.
Stage B
Prevent HF symptoms from starting & further cardiac
remodeling (already started)





Control symptoms
Improve Quality of Life
Prevent hospitalization & mortality
Stage D
Control symptoms, Improve Quality of Life
Reduce hospitalizations, establish “end of life” goals
Pharmacological Treatment: HFrEF
Stage A


ACEI/ARB: vascular disease,
CKD, or diabetes
Statins as appropriate
Stage B



ACEI or Entresto + BB + Ald Antag
If tolerated, do all.

Stage D
(“all”): ACEI/ARB, BB,
Entresto, Ald. Antag, BiDil,
Digoxin, Ivabradine,
Diuretics.
2nd Line/Select Pop.
First Line


Stage C
ACEI/ARB or Entresto
BB’s as appropriate
Add immediately once
symptoms are seen.


ARB, BiDil, Digoxin or Ivabradine
ARB only if ACEI not tolerated



Chronic Inotropes
Palliative care & hospice
Transplant
Last Line – Stage D

Chronic Inotropes
Pharmacological Treatment: HFpEF
(no drugs to help mortality!)
Diuretics: relieve symptoms of
congestion
Spironolactone & ARB: to decrease
hosplitalizations
Follow guidelines for comorbidities:
HTN, AFib, CAD, DM etc.
Pharmacologic Treatment



9 Major Classes: ACEI, BB, Sacubitril/Valsartan, Aldosterone Antag, ARB, Vasodilators, Sinus node
Inhibitor (Ivabradine), Digoxin, Diuretics.
Advanced HF Tx: Inotropes
Monitoring (All agents)
o Weight, BP, HR, Salt, Fluid, Electrolytes, Kidney, Liver, BNP, SE’s of meds.
HFrEF: Benefits of HF Agents
Mortality Benefits
(1st line)
ACEI/ARB’s
Beta Blockers
Aldosterone Antagonists
Sacubitril/Valsartan
Hydralazine/Isosorbide
Dinitrate (black ppl) (dilators)

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 Hospitalizations
(2nd line)
All w/ mortality benefits
Digoxin, Ivabradine
Hydralazine/Isosorbide
Dinitrate (black ppl) (dilators)
Symptom Relief


All agents listed
Diuretics (loop & thiazide)
ACE Inhibitors
(1st Line Agent)


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MOA
Benefit
Monitor
Adverse
Dosing
Interactions
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
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Inhibit AT1AT2, competitively bind to ACE
Prevent breakdown of bradykinin
Deters SNS activation:  vasoconstriction, PL & AL
Relieve symptoms (slower than diuretics)
Improve NYHA class and functional status.
 Hospitalizations, Mortality & Side Effects
 K, SCr and BUN w/ initiation or dose change
Paradoxical effect on kidneys: can  renal function
Hypotension, Hyperkalemia, Dry cough, Angioedema
CI: prev. anaphylaxis or angioedema w/ ACEI
o Bilateral renal artery stenosis (unilateral ok)
Start low and  as tolerated,  dose w/ renal disease.
Hypotension problem w/ hyponatremia
Benefit may not appear for several weeks
No tolerance w/ chronic use
Diuretics may act synergistically with ACEI’s
K supplements or agents that  K
NSAIDS
Hypotension w/ other anti-hypertensive agents.
Drugs
(target dose for survival benefit)

Captopril: 50mg TID

Quinapril: 20mg BID

Enalapril: 10-20mg BID

Fosinapril: 40mg daily

Lisinopril: 20-40mg daily

Ramipril: 10mg daily

Trandolapril: 4mg daily
ARB’s
(1st Line Agent – somewhat)


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MOA
Benefits
Adverse

competitively bind and block AT2-R
prevent vasoconstriction and aldosterone activation
pt intolerant to ACEI, just as effective
less evidence to support as 1st line agent
NOT a drug effect: Candesartan, Valsartan & Losartan (studied)
 pumping,  mortality.
 Hospitalizations, Mortality & Side Effects.
similar to ACEI profile
equal: Hypotension,  renal function & Hyperkalemia
lower rate: Angioedema
Drugs
(target dose for survival benefit)

Valsartan: 160mg BID

Losartan: 50-150mg daily

Candesartan: 32mg daily
ACEI/ARBs: K (w/ Ald. Antagonists even higher), avoid NSAIDs, hypotension
o Can worsen renal function
Beta Blockers
(1st Line Agent)

MOA
Benefit
Use
Dosing
Adverse
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Antag B adrenergic-R’s in heart & vasculature (restore variability,
prevent arrhythmia & remodeling)
Inhibit NE release & Renin secretion
Carvedilol: block beta1, beta2 & alpha-adrenergic receptors
Bisoprolol & Metoprolol: block beta1 adrenergic receptors
Symptom relief,  exercise tolerance & improve NYHA class.
More effective at maintaining ventricular response especially during
exercise (help HF patients with A Fib)
 Hospitalizations, Mortality & Side Effects
Consider for NYHA class 1 patients
Used in ALL pt’s in class 2 and 3 (unless specified)
If tolerated: class 4 patients
Shown to improve HF: Bisoprolol, Metoprolol Succinate & Carvedilol.
Start low,  as tolerated every 2 weeks. Taper off to avoid rebound
Not a rescue medication: benefit may take weeks
Added only once pt is hemodynamically stable
Initiate only if patient is euvolemic
Fluid retention & worsening HF @ 1st
Watch for weight increase and worsening signs of HF
Fatigue (try reducing dose or switching agent)
Bradycardia & Heart Block (decrease dose, look for drug interactions)
Hypotension (Carvedilol) (dizzy, lightheaded, blurry)
Drugs
(target dose for survival
benefit)

(1) Metoprolol Succ:
200mg daily

( & ) Carvedilol:
50mg BID

( & ) Carvedilol CR:
80mg daily

(1) Bisoprolol:
10mg daily
Aldosterone Antagonists
(1st Line Agent)

MOA





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Benefit
Dosing
Adverse

Competitively bind aldosterone-R’s in distal tubule & collecting duct
of the nephron
 Na & water reabsorption, as well as cardiac & vascular fibrosis
Symptom relief
 Hospitalizations, Mortality & Side Effects
start w/ 25mg daily, 50mg if symptoms persist
12.5mg if hyperkalemia develops
Eplerenone: $, reserved for gynecomastia patients
Hyperkalemia: risk w/ ACEI or K supplements & renal impaired
Gynecomastia: anti-androgen properties of Spironolactone
ACEI/ARBs: K (w/ Ald. Antagonists even higher)
Drugs
(target dose for survival benefit)

Eplerenone: 50mg daily

Spironolactone: 25mg daily/BID
Hydralazine/Isosorbide Dinitrate (BiDil)
(1st Line Agent – Vasodilator Class)
MOA
Benefit
Dosing
Adverse



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
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Unknown, synergistic effects
Isosorbide dilate by releasing nitric oxide.
Hydralazine mitigate tolerance to nitrates.
If ACEI/ARB not tolerated.
Possibly more effective than ACEI in black patients.
 Hospitalizations, Mortality & Side Effects.
Most decrease in mortality of agents so far.
Effects only with short acting dinitrate (not mononitrate)
1-2 Tablets TID
1 Tablet: 37.5mg hydralazine/20mg isosorbide dinitrate
BiDil
Resolved by d/c medication (headeache, dizzy, hypotension)
CI: phosphodiesterase-5-inhibitors (sildenafil, vardenafil etc) could result in severe
hypotension.
Sacubitril/Valsartan (Entresto)
(New 1st Line Agent)
MOA
Benefit
Dosing
Adverse

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Sacubitril: neprilysin inhibitor (neutral endopeptidase: NEP)
Valsartan: ARB
Together NP’s & Inhibit RAAS (ARNI)
Neprilysin also clears: Sub P, Bradykinin, AT1 & AT2
Add ARB to inactivate RAAS b/c of clearing AT2 & to angioedema.
Hospitalizations, Mortality & Side Effects
For CHF (NYHA classes 2-4) & EF: In place of ACEI/ARB
24/26mg, 49/51mg, 97/103mg (target dose)
If previously on ACEI/ARB start at 49/51mg
If naïve, start on 24/26mg BID
Do not administer with an ACEI or within 36hrs of last dose of ACEI.
CI: history of angioedema.
Healthy Heart

ANP/BNP: vasodilate, excrete
water and Na, fibrosis & cardiac
hypertrophy
Heart Failure
 BNP & neprilysin: NP’s,
vasoconstrict, water and Na
retention, fibrosis & cardiac
hypertrophy
Ivabradine
(2 Line Agent)
nd
MOA
Benefit
Dosing




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

Sinus node inhibitor
Selectively inhibit hyperpolarization of Na channel - SA & I current: regulates HR.
 Hospitalizations & Side Effects
For stable, symptomatic CHF with left ventricular EF 35% who are in sinus rhythm with resting HR 70.
Used if on max tolerated BB’s or have CI for BB use.
5mg, 7.5mg (target dose)
Start on 5mg BID. High risk for bradycardia: start on 2.5mg BID
Digoxin
(2nd Line Agent)
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MOA
Benefit
Dosage
Adverse
Monitor
Interactions 

Positive inotrope (mild), enhanced parasympathetic tone (calm down SNS)
Normal plasma ½ life: 36hrs with normal renal function.
Excreted primarily renally. If anuric: plasma ½ life – 5days!
Remain symptomatic even on ACEI/ARB, BB & diuretics
For HF patients with A Fib. (BB’s better w/ ventricular response during exercise)
 Hospitalization & Side Effects
Therapeutic Range: 0.5-2.0ng/mL
Goal in HF: 0.5-0.9ng/mL. Goal in A Fib: 1-2ng/mL
Monotherapy NOT appropriate! Do NOT abruptly d/c.
0.125-0.25mg daily. 0.125 in renal impaired/elderly. No loading dose needed.
Narrow TPW. Many Side Effects!
Elderly more sensitive, data showing negative effects in women ( mortality).
CI: Heart Block
Obtain serum digoxin levels, changing renal function, interacting drugs added to regimen.
Assessment of HF symptoms
Assessment of Digitalis toxicity: GI most common, neurological/neuromuscular, cardiac symptoms.
o Hypokalemia, hypomagnesemia, hypercalcemia.
Diuretics: can induce K and Mg loss.
Spironolactone: changes elimination,  digoxin concentrations.
Diuretics
(3 Line Agents)
rd
MOA
Benefit
Dosage
Adverse
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Inhibit reabsorption of electrolytes in the nephron.
o In loop Henle (loops)
o In distal tubule (thiazides)
Remove peripheral edema, pulm congestion
cardiac performance by circulatory overload
Most rapid symptoms of all agents. (hrs/days)
Won’t delay progression.
All patients with Stage C.
Monotherapy NOT appropriate!
Loops
Thiazides
Hyponatremia, Hypokalemia,
Hypomagnesia, uric acid,
renal dysfunction.
HYPOcalcemia


Hyponatremia, Hypokalemia,
Hypomagnesia, uric acid,
renal dysfunction.
HYPERcalcemia
Drugs
Thiazides: chlorthalidone & HCTZ less effective
in advanced disease.
Loops

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Ferosemide, Torsemide, Bumetanide
40: 20-10: 1
Potent & effective in all stages HF
Linear dose/response relationship
Remain effective in renal failure
Thiazide-Like



Metolazone (PO)
Chlorothiazide (IV)
Useful combo with Loops.
Inotropes
(Advanced HF Treatment Only)
MOA
Benefit



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
 Ventricular Filling Stroke Volume
 Palliation in end stage HF
 Used as a bridge to cardiac transplant
 Can  Mortality!!
Mirinone
Dopamine
Phosphodiesterase-3 Inhibitor
Strengthen HB & relax BV’s
Doesn’t  O2 demand (prefer: ischemia)
Better for severe HF w/ BB’s
Adverse: tachyarrhythmia, hypotension
& LFT’s
Dose: 0.125-0.75mcg/kg/min IV

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 heart function, may BP, help edema
Help w/ renal perfusion & ionotrophy
Tolerance may develop
Adverse: irregular heart rhythm,
tachyphylaxis, headache, nausea, tissue
necrosis.
Dose: 5-15mcg/kg/min IV
o Low: 2 “renal dose”
o Interm: 2-10 “beta dose”
o High: 10 “alpha dose”
Dobutamine

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 heart function, may BP
Tolerance faster than dopamine
Adverse: irregular heart rhythm (less),
tachyphylaxis, nausea, fever,
hypersensitivity
CI: sulfite allergy
Dose: 2.5-20 mcg/kg/min IV
Acute Decompensated Heart Failure


Sudden worsening (exacerbation) of HF symptoms leading to hospitalization
#1 cause hospitalizations in patients  65.
Patho
Causes
(either med or
disease related)
“always want to
control HTN”
Characteristics






 Cardiac output and/or cardiogenic pulmonary edema
Activation of sympathetic nervous system and RAAS
Compensatory mechanisms
Common: Nonadherence to chronic meds & Nonadherence to Na or fluid restrictions.
Uncontrolled BP, Acute MI, AFib/arrhythmias, drugs/alcohol/pulmonary embolus, infections
(-) Inotropic drugs: verapamil, nifedipine, diltiazem, BB’s

Drugs Na retention: steroids, thiazolidinediones, NSAIDs

Endocrine disorders: DM, hyperthyroidism, hypothyroidism


Other acute vascular disorders: valvular disease, endocarditis, myopericarditis, aortic dissection
Cardinal Symptoms: SOB, Edema, Fatigue


Elderly or near, equally male/female
Equally HFrEF/HFpEF: pEF (more female, uncontrolled HTN, older, but less CAD)

History of HTN + one of the following
o CKD, hyponatremia, hematological abnormalities, COPD
Congestion at Rest
Low Perfusion at Rest
Orthopnea ( 2 pillows), 12 JVP (can see it)
 Narrow Pulse Pressure
Pulmonary rates, S3 gallop, Edema
 Tachycardia with pulsus alternans
Pulm Capillary Wedge Pressure (PCWP): fluid
 Cool extremities, Hypotension
status,  30 mmHg
 Cardiac Index (CI): degree of perfusion,
proportional pulse pressure. 2.2 (cold)
Improve symptoms, restore normal oxygenation, optimize vol status, identify etiology
Address precipitating factors, optimize chronic oral therapy (discharge), minimize adverse effects
Identify patients who benefit from revascularization or a device
Identify risk of thromboembolism and need for anticoagulant therapy
Educate patients, consider initiating a disease management program
BB’s initiated AFTER volume status is optimal
o PO diuretics, vasodilators & inotropic agents should be d/c as well.
ACEI, ARB, Ald Antag, Entresto: held or reduced in pt with significant renal decline
Make sure standard therapy agents are restarted before discharge
o Follow up 7-14 days & telephone follow up after 3 days
Diagnosis

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Goals of Therapy
Chronic Therapy
Recommendations

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Symptomatic Classifications
Forrester Hemodynamic Classifications
Congestion at Rest
Pulm Capillary Wedge Pressure (PCWP) -fluid status (mid 18)
Warm & Dry - 1
Low Perfusion at Rest
Cardiac Index (CI)
(mid 2.2)


No additional therapy
Not a lot of edema or SE’s



IV Vasodilators (or Inotropes)
(+ IV fluids if too dry)
Not perfusing to organs well
Warm & Wet - 2


IV Diuretics (+/- Vasodilators)
Tons of fluid



IV Diuretics
+ IV Vasodilators (or Inotropes)
Not perfusing and accumulating fluid
Cold & Dry - 3
Cold & Wet - 4
Diuretic Therapy
Mainstay Therapy
Dosage




IV Loop’s: no difference b/w cont. inf. vs IV bolus (possibly cause hypokalemia)
2-2.5 times oral dose given IV intermittently
Double the dose if no response in 1st 6-8 hours
Switch to IV infusion if no response
o Monitor: urine output/renal function, electrolytes, symptoms, vitals, weight closely
o Furosemide (Lasix) 20mg IV = Furosemide 40mg PO (1 IV: 2 PO)
o Bumetanide & Torsemide (1 IV: 2 PO)
Adjuncts to Diuretic
Therapy If
Symptoms Persist
1.
Trial higher doses of IV loop if pt can tolerate
2.
Add thiazide-like or thiazide diuretic
a. Metolazone-PO (common before loop), Chlorothiazide-IV (allergic to sulfa etc) or HCTZ
3.
Add Ald. Antag.: Spironolactone or Eplerenone (watch for hyperkalemia)
4.
Add Vasopressin Antagonists: Conivalptan or Tolvaptan (not given often)
5.
Low-Dose (“renal dose”) Dopamine IV Infusion
6.
Ultrafiltration if diuretics fail (dialysis)
Vasopressin Antagonists

May consider short term: vol overloaded pts w/
persistent severe hyponatremia & at risk for symptoms
despite water restriction and optimal management.

Improves serum Na concentrations in hypervolemic,
hyponatremia states, but NO benefits long term.
Vasodilator Therapy
Uses

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 Absence of symptomatic hypotension. Only as adjuvant to Loop’s.
 Benefit: symptomatic relief ONLY!
 Caution w/ HFpEF bc more volume sensitive
IV Nitroglycerin (go to)
IV Na Nitroprusside (last line)
MOA: venodilate, preload & pulm
congestion
Best for HF & HTN, coronary ischemia, or
significant mitral regurgitation
Adverse: tachyphylaxis 24hr/resistance
Dose: 5-10mcg/min IV infusion
Can increment 5-10mcg Q 3-5min
Usual Range: 10-200mcg/min
Max Dose: 400mcg/min
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MOA: veno & arteriodilator, preload
& afterload
Awaiting transplant (limited use)
Adverse: hypotension & cyanide
toxicity (especially in renal failure)
Na thiosulfate – antidote
Dose: 5-10mcg/min IV infusion
Can increment 5-10mcg Q 5min
Usual Range: 5-300mcg/min
Dose 400 not recommended
IV Nesiritide (human BNP)
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MOA: LV filling pressure, variable
CO, urinary output & Na excretion.
Adverse: hypotension (bc long t ½)
Dose: 2mcg/kg IV bolus (optional)
followed by 0.01mcg/kg/min