Hf nurse ccreview2011

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  • Slide 11 The diagnosis of HF is a difficult one to make. Shortness of breath is a symptom associated with many disease states; physical examination is neither sensitive nor specific for CHF. One-third to one-half of patients with CHF have normal pumping function of the heart. Echocardiograms are useful for diagnosis of HF, and provide information to aid in estimating the ejection fraction. The procedure serves as an expensive means to rule in or rule out patients for HF. Echocardiograms are not always available, and require sophisticated technicians and interpretation.
  • Slide 19 The hemodynamic goal of therapy for the decompensated HF patient is mirrored by the clinical goals of relieving orthopnea, splanchnic congestions, edema, and jugular venous distention, while maintaining adequate pulse pressure and systolic blood pressure. When these goals cannot be achieved or sustained, invasive hemodynamic monitoring has often been performed for the purpose of confirming the hemodynamic profile and then guiding subsequent therapy to approach pulmonary capillary wedge (PCW), Right Atrial (RA), and systemic vascular resistance (SVR) goals.
  • Slide 20 The hemodynamic profiles of patients with advanced HF. The majority (90%) of patients presenting with acute decompensated HF are volume overloaded (“wet”). These patients may have cardiac index that is unchanged or decreased. Most patients with decreased cardiac index have elevated systemic vascular resistance, though a minority will have unchanged or low SVR. The signs and symptoms of congestion include orthopnea, jugular venous distention, and peripheral edema. Signs and symptoms of low perfusion include narrow pulse pressure, cool extremities, and decreased mental status.
  • Slide 27 Patients with HF frequently present to the hospital with worsened symptoms in a hypervolemic state. Therapy may initially target this excess fluid incorporating diuretics along with vasodilators to help reduce the overloaded state. Current therapies offer symptomatic benefits to patients with HF. Diuretics reduce fluid volume resulting in decreased pulmonary congestion and swelling of extremities. Vasodilators decrease blood vessel constriction, reducing preload and afterload, improving ventricular function and cardiac output. Inotropic agents stimulate the heart muscle, increasing contractility and cardiac output.
  • IV Agents for HF The relative benefits and possible limitations of IV HF therapies are summarized. Unlike other agents, including positive inotropes, nesiritide administration leads to a beneficial increase in cardiac output as well as decreases in PCWP and blood pressure, without affecting heart rate or rhythm. Young JB. Rev Cardiovasc Med . 2001;2(suppl 2):S19
  • Most Common IV Medications All Enrolled Discharges (N = 105,388) October 2001 –January 2004 The use of IV vasoactive medications is shown on this slide. IV diuretics are used in 88% of patients admitted with ADHF. Data on file, Scios Inc.
  • Slide 21 The hemodynamic profiles of patients with advanced HF. The majority of patients with heart failure are volume overloaded (“wet”). These patients may have cardiac index that is unchanged or decreased. Most patients with decreased cardiac index have elevated systemic vascular resistance, though a minority will have unchanged or low SVR. Vasodilators would be expected to have therapeutic benefits in the “wet and warm” and the majority of “wet and cold patients.” While intravenous intropic therapy is often employed to reduce filling pressures and improve cardiac output, intravenous vasodilator therapy in the setting of vasoconstriction can often achieve similar results without the risks of aggravating ischemia and arrhythmias, and with easier transition to oral vasodilator regimens. Patients with signs of systemic hypoperfusion that are “dry” would be expected to have therapeutic benefits with volume loading and/or inotropic agents.
  • Limitations of Traditional Vasodilators Traditional vasodilator therapy has limitations. Nitroglycerin is associated with an increase in tachyphylaxis and headache. Nitroprusside is associated with, among other events, an increase in plasma renin activity and production of toxic metabolites. Fonarow GC. Rev Cardiovasc Med . 2002;3(suppl 4):S18
  • In contrast to nesiritide, the onset of a NTG-mediated hemodynamic effect was delayed, and despite aggressive up-titration the reduction in PCWP was gradually attenuated due to early development of tolerance. IV NTG, at a mean dose of 41 ± 20.3 μg/min at 15 minutes and 77.8 ± 54.3 μg/min at 30 minutes had no significant effect. Up titration of NTG to 146 ± 77 μg/min by 2 hours, resulted in a maximum reduction of PCWP (6.8  5.6 mm Hg; p=0.007). Despite further increase to 160.6 ± 67.5 μg/min, the effect of NTG diminished over time with only 3.2  7.0 mm Hg reduction of PCWP at 24 hours (p=0.15) compared to 12.2  7.5 mm Hg with nesiritide (p<0.001 vs. baseline and 0.005 vs. NTG). The findings of the study, therefore, demonstrate an advantage of nesiritide and reemphasize the limitations of NTG in the treatment of patients hospitalized for decompensated heart failure. Reference : Uri Elkayam et al. Difference In Effect On Left Ventricular Filling Pressure Between Intravenous Nesiritide And High Dose Nitroglycerin In Patients With Decompensated Heart Failure. Am J Card. 2004: 93; 237-240.
  • ADD HAZARD RATIO as TEXT BOX
  • keep the order of subgroups as the death/readmission Add back the N’s to the subgroups Confirm which subgroups markedly/moderately ???
  • keep the order of subgroups as the death/readmission Add back the N’s to the subgroups Confirm which subgroups markedly/moderately ???
  • keep the order of subgroups as the death/readmission Add back the N’s to the subgroups Confirm which subgroups markedly/moderately ???
  • Jon– Make a new slide with the “cumulative distribution for change in creatinine” at end of treatment and discharge
  • Hf nurse ccreview2011

    1. 1. Acute Heart Failure Allen S. Anderson, M.D., FACC Director, Heart Failure Program Medical Director of Cardiac Transplantation Associate Professor of Medicine University of Chicago Medical Center Diagnosis and Treatment The C enter for H eart F ailure Management
    2. 2. Diagnosis of CHF: Clinical Challenge <ul><li>Symptoms and signs of heart failure like shortness of breath and edema have a broad differential diagnosis </li></ul><ul><li>Physical exam is neither sensitive nor specific for CHF and, even in good hands, there are often errors </li></ul><ul><li>CXR findings have limited accuracy for CHF </li></ul><ul><li>One-third to one-half of patients with CHF have normal systolic function </li></ul>Maisel A. et al. J Am Coll Cardiol 2001;37(2):379-85
    3. 3. Goals for Therapy of Acute Decompensated Heart Failure Absence of orthopnea No peripheral edema No hepatomegaly/ascites Valsalva square wave absent Jugular venous pressure < 8 cm Warm extremities Systolic blood pressure > 80 SBP-DBP/SBP > 0.25 Pulmonary capillary wedge pressure < 15 mmHg Right atrial pressure < 8 mmHg Systemic vascular resistance < 1200 dynes-sec-cm -5 Systolic blood pressure > 80 mmHg Assessed Clinically Measured Directly Stevenson LW. Eur J Heart Failure 1999;1:251-257
    4. 4. The Physical Exam As A Diagnostic Test From Ewy, McIntyre et al, Stevenson & Perloff, Zema et al. PCWP>20- 22 mmHg Sensitivity Specificity Can’t tell Orthopnea 90% 95% JVP inc. 80% 98% 15% Valsalva 90% 90% 25% HJ Reflux 92% 81% ? Perip edema 25% 95% 5% Rales 15% 95%
    5. 5. Invasive Hemodynamic Assessment <ul><li>Invasive </li></ul><ul><li>Significant Complications </li></ul><ul><li>Expensive </li></ul><ul><li>Requires ICU or Cath Lab setting </li></ul><ul><li>Data sometimes difficult to interpret </li></ul>
    6. 6. Goals of Acute HF Therapy <ul><li>Alleviate symptoms </li></ul><ul><li>Treat volume overload </li></ul><ul><li>Preserve/improve end organ function </li></ul><ul><li>Limit hospitalization </li></ul><ul><li>Initiate/optimize chronic therapy </li></ul><ul><li>Prevent readmission </li></ul><ul><li>Improve long-term outcomes </li></ul>
    7. 7. Rapid Assessment of Hemodynamic Status <ul><li>Congestion at Rest </li></ul>Low Perfusion at Rest C NO NO YES YES L A B Warm & Dry Warm & Wet Cold & Wet Cold & Dry ( C omplex) ( L ow Profile) Signs/Symptoms of Congestion: Orthopnea / PND JV Distension Hepatomegaly Edema Rales (rare in chronic heart failure) Elevated est. PA systolic Valsalva square wave Possible Evidence of Low Perfusion: Narrow pulse pressure Cool extremities Sleepy / obtunded Hypotension with ACE inhibitor Low serum sodium Renal Dysfunction (one cause)
    8. 8. Current Treatment of Acute Heart Failure Diuretics Aquaretics Ultrafiltration Reduce fluid Volume Na + & H 2 0 Vasodilators Decrease Preload And Afterload Inotropes Augment Contract- ility
    9. 10. Diuretic Resistance <ul><li>Poor oral absorption due to gut edema </li></ul><ul><li>Decreased perfusion of kidney results in decreased delivery of loop diuretics </li></ul><ul><li>Decreased GFR results in decreased filtered load of sodium </li></ul><ul><li>Volume depletion activates plasma renin activity and stimulates SNS </li></ul><ul><li>Increased proximal tubule reabsorbtion of sodium, particularly in setting of elevated AII and elevated catecholamine levels </li></ul><ul><li>Increased distal reabsorbtion of sodium, stimulated by aldosterone </li></ul><ul><li>Associated with tubular hypertrophy: resetting basal rates of sodium reabsorbtion. </li></ul>
    10. 11. Diuretic Principles <ul><li>The right dose is what it takes to effect diuresis </li></ul><ul><ul><li>as high as it takes </li></ul></ul><ul><ul><li>as low as you can </li></ul></ul><ul><li>High dose loop vs loop+metolazone </li></ul><ul><li>Continuous IV infusion of loop diuretic </li></ul><ul><li>Flexible dosing </li></ul><ul><li>Daily weights </li></ul>
    11. 12. Change in Weight From Admission to Discharge The ADHERE Registry First Quarter 2002 Benchmark Report. 2002:29
    12. 13. Primary End Point Weight Loss at 48 Hr Primary End Point Weight Loss at 48 Hr
    13. 14. Freedom From Re-hospitalization for Heart Failure
    14. 15. Intravenous Agents for Heart Failure  increase;  decrease; + effect (number of and qualitatively associated with degree of effect); 0 no effect Reference: Adapted from Young JB. Rev Cardiovasc Med .2001;2(suppl 2):S19. Therapy CO PCWP BP HR Arrhy thmia Shorter Onset Longer Offset Dopamine (ng/kg/min) Low (<3) Mod (3 –7) High (7–15)                +++ +++ +++ 0 0 0 Dobutamine      +++ 0 Milrinone      + ++ Nitroglycerin      +++ 0 Nesiritide      ++ ++ Nitroprusside      ++++ 0
    15. 16. Most Common IV Medications All Enrolled Discharges (n=105,388) October 2001-January 2004 0 10 20 30 40 50 60 70 80 90 100 Patients (%) IV Diuretic Dobutamine Dopamine Milrinone Nesiritide Nitroglycerin Nitroprusside IV Vasoactive Meds 88% 6% 6% 10% 3% 1% 10%
    16. 17. Profiles and Therapies of Advanced Heart Failure Yes R. Bourge, UAB Cardiology (adapted from L. Stevenson) Stevenson LW. Eur J Heart Failure 1999;1:251-257 No Warm and Dry PCW and CI normal Warm and Wet PCW elevated CI normal Cold and Wet PCW elevated CI decreased Cold and Dry PCW low/normal CI decreased Vasodilators Nitroprusside Nitroglycerine Nesiritide Inotropic Drugs Dobutamine Milrinone Calcium Sensitizers Nl SVR High SVR Congestion at Rest Low Perfusion at Rest No Yes
    17. 18. Limitations Of Traditional Vasodilators Reference: Fonarow GC. Rev Cardiovasc Med. 2002;3(suppl 4):S18 <ul><li>Tachyphylaxis </li></ul><ul><li>Headache </li></ul><ul><li>Underdosed </li></ul><ul><li>Titration required </li></ul>Nitroglycerin Nitroprusside <ul><li>Difficult titration </li></ul><ul><li>ICU ( ± arterial line) </li></ul><ul><li>Coronary “steal” </li></ul><ul><li>Toxic metabolites </li></ul><ul><li>Increased renin </li></ul>
    18. 19. Nitroglycerin dose and change in PCWP during treatment with Nitroglycerin 0 20 40 60 80 100 120 140 160 180 0 3 6 9 12 15 18 21 24 Time (hours) NTG dose (micrograms/min) -8 -7 -6 -5 -4 -3 -2 -1 0 Change in PCWP (mmHg) NTG Dose Change in PCWP * * * * * * [n=9 (<3 hrs); n=12 (>3 hrs)] U. Elkayam et al. Am J Card. 2004: 93; 237-240 * p<0.05 versus baseline
    19. 20. VMAC Trial: Hemodynamic Improvement References: 1. Publication Committee for the VMAC Investigators (Vasodilation in the Management of Acute CHF). Intravenous nesiritide vs nitroglycerin for the treatment of decompensated congestive heart failure: a randomized controlled trial. JAMA . 2002;287:1531-1540. 2. NATRECOR ® Full Prescribing Information. Nitroglycerin Nesiritide Placebo BL 1 2 3 -10 -9 -8 -7 -6 -5 -4 -3 -2 -1 0 # p < 0.05 versus placebo * p < 0.05 versus NTG  # * # *  # *  # # # *  Time (hours) Mean Change from Baseline (mm Hg) (All Treated Catheterized Patients, as Randomized)
    20. 21. Randomized (n=7141) Study population-ASCEND Placebo MITT=3511 <ul><li>Placebo (n=3577) </li></ul><ul><li>  Did not receive study drug (n=66) </li></ul><ul><li>Hypotension (n=28) </li></ul><ul><li>Exclusion criteria (n=8) </li></ul><ul><li>Physician decision (n=6) </li></ul><ul><li>Participant withdrew consent (n=14) </li></ul><ul><li>Other reason (n=10) </li></ul>Nesiritide MITT=3496 <ul><li>Nesiritide (n=3564) </li></ul><ul><li>Did not receive study drug (n=68) </li></ul><ul><li>Hypotension (n=26) </li></ul><ul><li>Exclusion criteria identified (n=9) </li></ul><ul><li>Physician decision (n=6) </li></ul><ul><li>Participant withdrew consent (n=16) </li></ul><ul><li>Other reason (n=11) </li></ul>
    21. 22. Co-Primary outcome: 30-day all-cause mortality or HF rehospitalization Placebo Nesiritide HF Rehospitalization 30-day Death/HF Rehospitalization 30-day Death 0 2 4 6 8 10 12 Risk Diff (95 % CI) -0.7 (-2.1; 0.7) -0.4 (-1.3; 0.5) -0.1 (-1.2; 1.0) % 10.1 4.0 6.1 Hazard Ratio 0.93 (95% CI: 0.8,1.08) P=0.31 9.4 3.6 6.0
    22. 23. 30 day death/HF readmission subgroups Difference (%) and 95% Confidence Interval Risk Difference <1: Favors Nesiritide; Risk Difference >1: Favors Placebo All Subjects N=6836 Sex Female Male N=2335 N=4501 Age ≤ 64 65-74 ≥ 75 N=3029 N=1774 N=2033 Race White Black or African American Asian Other N=3849 N=1018 N=1671 N= 297 Region North America Latin America Asia-Pacific Central Europe Western Europe N=3098 N= 644 N=1668 N= 956 N= 470
    23. 24. 30 day death/HF readmission subgroups Difference (%) and 95% Confidence Interval Risk Difference <1: Favors Nesiritide; Risk Difference >1: Favors Placebo All Subjects N=6836 Baseline SBP (mmHg) < 123 ≥ 123 N=3346 N=3490 Baseline Ejection Fraction (%) <40 ≥ 40 N=4362 N=1187 Renal function- MDRD GFR (mL/min/m 2 ) <60 ≥ 60 N=3395 N=3093 History of CAD No Yes N=3092 N=3742 History of Diabetes Mellitus No Yes N=3923 N=2913
    24. 25. 30 day death/HF readmission subgroups Difference (%) and 95% Confidence Interval Risk Difference <1: Favors Nesiritide; Risk Difference >1: Favors Placebo All Subjects N=6836 Inotrope Use at Randomization No Yes N=6556 N=280 Vasodilators None Any IV Vasodilators No IV Nitroglycerin IV Nitroglycerin N=5889 N=942 N=5943 N=892 Diuretic Use from Hosp through Rand No Yes N=691 N=6145 Study Drug Bolus No Yes N=2609 N=4227 Time from Hosp to Rand <15.53 ≥ 15.53 N=3426 N=3410
    25. 26. Co-Primary Endpoint: 6 and 24 hour dyspnea 70 60 50 40 30 20 10 0 10 20 30 40 % Subjects 24 Hours Markedly Better Minimally Worse Moderately Better Moderately Worse Minimally Better Markedly Worse No Change 70 60 50 40 30 20 10 0 10 20 30 40 % Subjects 50 60 6 Hours 42.1% 44.5% 66.1% 68.2% 3444 Placebo 13.4 28.7 34.1 21.7 P=0.030* 3416 Nesiritide 15.0 29.5 32.8 20.3 3398 Placebo 27.5 38.6 22.1 9.5 3371 Nesiritide 30.4 37.8 21.2 P=0.007* 8.6
    26. 27. OR <1: Favors Placebo; OR >1: Favors Nesiritide; Odds Ratio of Markedly/Moderately vs. Other 24 hours 6 hours Dyspnea at 6 and 24 Hours Odds for Moderate-Marked Improvement All Subjects N=6860 N=6769 Sex Female Male N=2343 N=4517 N=2308 N=4461 Age ≤ 64 Years 65-74 Years ≥ 75 Years N=3064 N=1779 N=2017 N=3011 N=1761 N=1997 Race White Black Asian Other N=3815 N=1022 N=1722 N=300 N=3758 N=1009 N=1702 N=299 Region North America Latin America Asia-Pacific Central Europe Western Europe N=3074 N=636 N=1719 N=962 N=469 N=3026 N=639 N=1698 N=949 N=457
    27. 28. 24 hours 6 hours Dyspnea at 6 and 24 Hours Odds for Moderate-Marked Improvement OR <1: Favors Placebo; OR >1: Favors Nesiritide; Odds Ratio of Markedly/Moderately vs. Other All Subjects N=6860 N=6769 SBP <123 ≥ 123 N=3369 N=3491 N=3314 N=3455 GFR <60 ≥ 60 N=3494 N=3121 N=3349 N=3075 Ejection Fraction <40 ≥ 40 N=4385 N=1186 N=4335 N=1171 CAD No Yes N=3115 N=3743 N=3082 N=3685 Diabetes No Yes N=3930 N=2930 N=3887 N=2882
    28. 29. 24 hours 6 hours Dyspnea at 6 and 24 Hours Odds for Moderate-Marked Improvement OR <1: Favors Placebo; OR >1: Favors Nesiritide; Odds Ratio of Markedly/Moderately vs. Other All Subjects N=6860 N=6769 Inotropes No Yes N=6574 N=286 N=6481 N=288 Vasodilators None Any IV Vaso No IV Nitro IV Nitro N=5912 N=943 N=5965 N=894 N=5835 N=929 N=5886 N=882 Diuretics No Yes N=691 N=6169 N=679 N=6090 Study Medication Bolus No Yes N=2612 N=4248 N=2564 N=4205 Time from Hosp to Rand <15.53 ≥ 15.53 N=3428 N=3432 N=3369 N=3400
    29. 30. Secondary endpoints Placebo (n=3511) Nesiritide (n=3496) Difference (95% CI) P-value Persistent or worsening HF or all-cause mortality through discharge 4.8% (165) 4.2% (147) -0.5 (-1.5 to 0.5) 0.30 Days alive and outside of hospital through Day 30 20.7 20.9 0.2 (-0.13 to 0.53) 0.16 CV death or CV rehosp through Day 30 11.8% (402) 10.9% (372) -0.9 (-2.4 to 0.6) 0.24
    30. 31. Wellbeing at 6 and 24 hours (markedly/moderate ) 3383 Placebo 3364 Nesiritide 24 Hours Markedly Better Minimally Worse Moderately Better Moderately Worse Minimally Better Markedly Worse No Change 70 60 50 40 30 20 10 0 10 20 30 40 % Subjects 50 60 70 60 50 40 30 20 10 0 10 20 30 40 % Subjects 50 60 P=0.318 P=0.018 12.2 13.2 28.1 28.2 34.6 33.9 22.9 22.0 24.9 27.1 38.8 38.6 23.6 22.6 9.8 9.2 3430 Placebo 3406 Nesiritide 6 Hours
    31. 32. Renal Safety Anytime Through Day 30 Placebo (n=3509) Nesiritide (n=3498) P-value >25% decrease eGFR 29.5% 31.4% 0.11 End of Treatment Creatinine Creatinine (mg/dL) Cum Dist 0 2 4 6 8 0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1.0 Discharge or 10 day Creatinine Creatinine (mg/dL) Cum Dist 0 2 4 6 8 0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1.0 Nesiritide Placebo
    32. 33. Hypotension Placebo (n=3509) Nesiritide (n=3498) Risk Difference (95% CI) P- value Any hypotension (Through Day 10/discharge) 15.3% (538) 26.6% (930) 11.3 (9.4 to 13.1) <.001 Asymptomatic Hypotension 12.4% (436) 21.4% (748) 9.0 (7.2 to 10.7) <.001 Symptomatic Hypotension 4.0% (141) 7.1% (250) 3.1 (2.1 to 4.2) <.001
    33. 34. 30-day mortality meta-analysis 1 10 0.1 Odds Ratio (95% CI) COMBINED 30 day w/out ASCEND 1.28 (0.73, 2.25) PROACTION (N=237) 6.93 (0.89, 53.91) Mills (N=163) 0.38 (0.05, 2.74) Efficacy (N=127) 1.24 (0.23, 6.59) Comparative (N=175) 1.43 (0.50, 4.09) PRECEDENT (N=147) 0.59 (0.18, 2.01) VMAC (N=498) 1.63 (0.77, 3.44) ASCEND-HF (N=7007) 0.89 (0.69, 1.14) COMBINED with ASCEND 1.00 (0.76, 1.30)
    34. 35. University of Chicago Center for Heart Failure Management Cardiac Transplant Service Allen S. Anderson, M.D., FACC Director, Center for Heart Failure Medical Director Transplant Service Valluvan Jeevanandam, M.D. Chief, Cardiothoracic Surgery Surgical Director Transplant Service Transplant Coordinators Catherine Murks, RN, CNP Rosalind Davis, RN Heart Failure Coordinators Elinor Lowry, RN Barbara Valentine-Bates, RN Transplant Social Worker Rina Murao, LCSW

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