O GoConqr está de visual novo! Conte para nós o que você achou.

Flashcards

sept 9

Shylla T Inglês 96 flashcards

Flashcards do conjunto (96)

  1. 1Systolic failurea defect in the contraction -> reduced ejection fraction. common among the younger patients
  2. 2Diastolic failureinadequate relaxation -> reduced filling of the heart and reduced
    cardiac output.
    The ejection fraction can be normal even though stroke volume is significantly
    reduced. The proportion of patient with diastolic failure increases with age
  3. 3Causes of Heart FailureCoronary heart disease
    Hypertension
    Diabetes
  4. 4Chronic Heart FailureDiuretics
    - Aldosterone antagonist
    - ACE inhibitors
    - Angiotensin receptor blockers
    - β-blockers
    - Cardiac glycoside (digoxin)
    - Vasodilators
    - hyperpolarization-activated
    cyclic nucleotide-gated channel
    blocker
  5. 5Acute Heart FailureDiuretics
    - Vasodilators
    - β-agonists
    - Bipyridines
    - Natriuretic peptide
  6. 6Mechanism of action:No direct effect on the heart
    - Induce loss of sodium and water -> ameliorate:
    - edema
    - venous pressure and ventricular preload
  7. 7Spironolactone antagonizesaldosterone’s profibrotic effect on the
    heart and blood vessels.
  8. 8Effect on potassium control:Furosemide and Hydrochlorothiazide: loss of potassium
    Amiloride and Spironolactone : potassium retention
  9. 9Neprilysin inhibitorsSacubitril
  10. 10SacubitrilFirst neprilysin inhibitor; given in combination of valsartan
  11. 11Mechanism of actionSacubitril is metabolized in a neprilysin inhibitor
    - Protects vasoactive peptides (natriuretic peptides, bradykinin, adrenomedulin) from degradation
    - decrease vasoconstriction, sodium retention, and fibrosis
  12. 12Therapeutic usereduce cardiovascular death in and heart failure hospitalization in patients with heart failure with reduced ejection fraction
  13. 13Side effectsHypotension, hyperkalemia
    angioedema
  14. 14β adrenoceptor blockersOnly three drugs in that class are approved by the FDA for the indication of heart failure:
    Bisoprolol, Carvedilol, Metoprolol succinate
  15. 15Mechanism of actionReduce heart rate, improve relaxation
    - Reverse apoptotic effect of catecholamines
    - Reduce tissue remodeling
    - Reduce renin production and release
  16. 16Carvedilol Mechanism of action:beta1 and beta2 blocker
    alpha1 blocker: vasodilation
    anti-inflammatory properties
    anti-apoptotic properties
  17. 17Mechanism of action:potent inhibitors of cellular Na+/K+-ATPase
    - increase intracellular sodium
    - accumulation of intracellular calcium via the Na+/Ca++ exchange
  18. 18Mechanism of action:parasympathomimetic action of digitalis
    - reduces sinoatrial firing rate (negative chronotropy)
    - reduces conduction velocity of electrical impulses through the atrioventricular node (negative dromotropy)
  19. 19Therapeutic use:Primarily heart failure
    Atrial fibrillation and flutter
  20. 20Side effects:Cardiac arrhythmia, especially atrial tachycardia and atrioventricular
    block.
    Dizziness, confusion, visual disturbances (blurred yellow vision: xanthopsia)
  21. 21part 2Digitalis compounds are contraindicated in patients who are hypokalemic, or who have atrioventricular block or Wolff-ParkinsonWhite (WPW) syndrome.
    Reverse toxicity: immune Fab (Digibind) or potassium
  22. 22hyperpolarization-activated cyclic nucleotidegated channel blockerIvabradine
  23. 23Ivabradineextensively metabolized in the liver and intestines by CYP3A4
  24. 24Mechanism of action:inhibits the If sodium current, resulting in heart rate reduction
  25. 25Therapeutic use:Chronic heart failure with a resting heart rate of at least 70 beats per
    minute
  26. 26Side effectsFetal toxicity, atrial fibrillation, bradycardia
    Phosphenes (effect on retinal ion channels)
    No changes in: ventricular repolarization, myocardial contraction,
    blood pressure.
  27. 27DopamineBiosynthetic precursor of norepinephrine
    Stimulate norepinephrine release
  28. 28low dosesstimulates the heart and decreases systemic vascular resistance
    dopamine binds to D1 receptor in kidney: vasodilation
  29. 29High dosesdopamine binds to α1 receptors: vasoconstriction
  30. 30Dobutaminereceptor Selectivity: β1 > β2 > α1
    sympathomimetic amine that is an inotropic agent by augmenting
    stroke volume.
  31. 31Mechanism of actionActivate adenylate cyclase
  32. 32Therapeutic use:Acute heart failure
  33. 33Side effectsArrhythmia, angina
    Headache, tremor
    Also nausea for dopamine
  34. 34Inamrinone and Milrinone Mechanism of action:Phosphodiesterase inhibitor
    in the heart and blood vessels
  35. 35Therapeutic use:Short-term IV therapy of acutely-decompensated heart failure
  36. 36Side effectsNausea and vomiting
    Arrhythmia
    Thrombocytopenia
    Liver toxicity
    Milrinone seems less toxic except for arrhythmia.
  37. 37Nesiritidethe recombinant form of the 32 amino acid human Btype natriuretic peptide (IV administration), which is normally
    produced by the ventricular myocardium
  38. 38Mechanism of actionincreasing intracellular cGMP -> smooth muscle cell relaxation.
    Reduces pulmonary and arterial blood pressure.
    promotes vasodilation, natriuresis, and diuresis.
  39. 39Therapeutic useacutely decompensated congestive heart failure with dyspnea at rest
    or with minimal exertion.
  40. 40Side effects:Renal damage, hypotension, headache, (may increase mortality).
  41. 41pathoImpairs the ability of the ventricle to fill or eject
  42. 42Sigs and symptomsdyspnea, fatigue, exercise intolerance, abdominal bloating, early satiety, and peripheral edema
    Maybe d/t disorders of pericardium, heart valve, myocardium, coronary circulation
    or rhythm disturbances
     Etiologies of LVSD
  43. 43 Etiologies of LVSDCAD, idiopathic dilated CM,
  44. 44how to diagnose HFclinical dignosis
    Chronicity, severity and degree of hemodynamic decompensation and specific factors such as age, gender and other comorbidities influence signs and
    symptoms.
    combine clinic with lab/imaging (confirm)
  45. 45NYHAused to assess exercise tolerance and should be determined in the ambulator and compensated state.
    I = No symptoms
    II = Symptoms with moderate or marked levels of activity
     III = Symptoms with mild activity
     IV = Symptoms at rest
  46. 46Physical exam should focus **imporant in diagnose HFon hemodynamic status along with 2 axes: degree of volume overload (“wet” or “dry”) and adequacy of perfusion (“warm” or “cold”)
  47. 47Evidence of fluid overload:elevated JVP, hepatojugular reflux, gallops (S3 and S4), murmurs of TR or MR, pulmonary rales, hepatomegaly, ascites and edema
  48. 48ways to dignoseEKG, full laboratory assessment and CXR to be performed in all pts presenting with
    HF
  49. 49BNP or NT-pro BNPwhen pts presenting with dyspnea is uncertain.
    Good negative predictive values to exclude HF and also a prognostic indicator.
  50. 50Coronary angiographyshould be performed in pts with new onset HF
  51. 51 Endomyocardial biopsyreserved for pts with specific dx (hemochromatosis, amyloidosis, sarcoidosis)
  52. 52Cause of decompensation should be explored and define hemodynamic profileWet vs. dry and warm vs. cold.
    Provides prognostic information and basis for treatment plan
  53. 53Mgmt of ADHF can be divided into 2 temporal periodsAcute period identifying precipitating factors, improving symptoms and addressing role of comorbidities in the acute decompensation
    Transition time to outpatient setting
  54. 54Most patients are wet and warm. Hence,relieve the congestion
     IV loop diuretics will produce a diuresis with decrease in filling pressures
     Also exerts vasodilatory effect
     Dose should be doubled from outpatient setting
  55. 55Morphineinduced vasodilation and relieves breathlessness as well as anxiety
  56. 56 Supplemental O2should be initiated
    NPPV if necessary
  57. 57Vasodilatory therapyto be initiated in the abscess of symptomatic hypotension
    Short acting ACEI, ARB or hydralazine
  58. 58Nitroprusside if need foracute combined afterload and preload reduction (hypertensive emergency, acute AR and acute MR)
  59. 59 Nesiritide.
  60. 60Tolvaptanis a vasopressin V2 receptor antagonist
    Failed to show reduction in all cause morality or HF hospitalization.
    Approved by FDA for severe and/or symptomatic hyponatremia in pts with HF.
  61. 61IV inotropic agents (dobutamine, milrinone, dopamine)to be used if systemic hypoperfusion
     Benefits outweigh risks of arrhythmias and increase in O2 demand
     Surveillance in ICU
  62. 62Temporary mechanical circulatory assistanceif not responding to pharmacologic therapy
    Help “bridge” appropriate pts to long-term mechanical circulatory support to cardiac
    transplantation
    Continuous electrocardiographic monitoring
  63. 63chronic mangementOptimize pharmacologic regimen
    Goal shifts to enhancing survival, minimizing symptoms and disability, improving functional capacity and delaying disease progression.
    All pts should receive dietary instructions (daily sodium restrictions), fluid restriction, record daily weights, and diuretic mgmt when weight gain
  64. 64Renal insufficiency complicating HF mgmtcardiorenal syndrome
    HF pts already have baseline impaired renal function
  65. 65Worsened HF decline in renal perfusion low response to diuretics. then u have toUse higher doses of diuretics or diuretics with synergistic effects
    If diuretics are ineffective or complicated by progressive renal insufficiency, then mechanical fluid removal
  66. 66THERAPIES FOR HF WITH LEFT VENTRICULAR SYSTOLIC DYSFUNCTIONDiuretics treat sodium and fluid retention
     ACEI are vasodilators and potent neurohormonal antagonists
    ARB if ACEI intolerant
    Neprilysin
  67. 67Neprilysinneutral endopeptidase that degrades endogenous vasoactive peptides (natriuretic peptides, bradykinin and adrenomedullin)
  68. 68part 2BB decrease the symptoms of HF and reduce risk of death and hospitalization
    Aldosterone receptor antagonists (spironolactone and eplerenone)
  69. 69Aldosterone receptor antagonistshave shown to reduce mortality and hospitalization and improve functional class in pts with advance HF.
  70. 70DISEASE MANAGEMENT STRATEGIES AND QUALITY IMPROVEMENTPrevention of HF hospitalization is a primary benefit of multidisciplinary disease
    mgmt program.
    HF pts with multiple readmissions, moderate to severe HF, multiple comorbidities should be referred.
    Multidisciplinary team made up of physicians, HF nurses, dieticians and pharmacist and family members
  71. 71part 2Hospitalist play a critical role in leading transition from inpatient to outpatient care.
    Educate patients with HF and their families is critical
  72. 72EXERCISE TRAINING AND CARDIAC REHABILITATIONExercise training in pts with HF have been showed to be safe and effective in
    improving functional capacity, exercise tolerance, quality of life, reducing
    hospitalization and improving survival
  73. 73HFPEF Previously known as diastolic HF
     Half of pts with HF have preserved LVEF
     Increasing d/t to aging population, increasing incidence of HTN and DM
  74. 74part 2Rate of hospitalization and death rates are similar to HFrEF
    More likely older, female, hx of HTN and a-fib
    In contrast to HFrEF, HFpEF has been studied in fewer clinical trials and no tx to
    date has been shown to improve survival in this type of HF
  75. 75plays role in HFpEFReduced diastolic ventricular compliance and abnormal relaxation. Abnormal
    renal sodium and water handling, reduced vascular compliance and anemia
  76. 76Several myocardial disordermaybe present as HFpEF including restrictive (infiltrative) and hypertrophic CMs
  77. 77May have difficulty tolerating a-fib due toloss of atrioventricular synchrony
    -reduce LV stroke volume.
  78. 78INITIAL MGMTOccult coronary heart disease is reversible cause of diastolic HF and should be
    excluded in pts with angina.
    Identification and tx of obesity, anemia and sleep disordered breathing are important
    ARB may decrease hospitalized in HFpEF
  79. 79DISEASE MANAGEMENT STRATEGIESSimilar to HFrEF, high-risk HFpEF pts should be referred to HF mgmt.
    Multidisciplinary approach.
    Discharge once optimal volume status, symptoms have resolved and appropriate
    meds have controlled HR and BP w/o hypotension or renal insufficiency
    Close f/u with a PCP or cardiologist within a week
  80. 80Lifestyle InterventionsAvoid the bad stuff: no smoking, alcohol, or street drugs
    Limit salt to < 3 grams/day
    Limit fluid to < 2 liters/day if symptomatic with volume overload
    Weight loss if patient is obese
    Fish oil? (GISSI-HF trial)
  81. 81Which Medications Reduce Mortality in CHFrEFbeta blockers
    give more dose of it
  82. 82Which Medications Reduce Mortality in CHFrEFAce inhibitor:
    Angiotensin receptor blocker:
    Beta blocker:
    Alternative to ACE/ARB: hydralazine + isosorbide mono/di nitrate
  83. 83Why use the newer medications?Comprehensive regimen (ARNI, MRA and SGLT2 inhibitor + beta blocker) performed better than traditional CHF regimen (ACEi or ARB + beta blocker)
    Reduced hospital admission for heart failure (hazard ratio [HR] 0.32, 95% CI 0.24-0.43)
    Decreased in all-cause mortality (HR 0.53, 95% CI 0.40-0.70).
    PARADIGM-HF, EMPHASIS-HF, DAPA-HF
  84. 84ARNI (Angiotensin Receptor / Neprilysin Inhibitor)Sacubitril valsartan
    PARADIGM-HF, comparing ARNI with ACE inhibitor
  85. 85Mineralcorticoid Antagonists (=Aldosterone Antagonists)Spironolactone
    Also blocks androgen receptors
    Eplerenone
    More specific for aldo receptor, so less gynecomastia / breast tenderness
    *Both cause hyperkalemia
  86. 86Effect of SGLT 2 InhibitorsReduction in HF exacerbations requiring hospitalization (31% RRR or 3% ARR)
    Side effects: genital infections, DKA
  87. 87Symptom ReliefDigoxin
  88. 88DigoxinCardiac glycoside, oldest CHF medication
    Increases inotropy
    prevents clinical deterioration and hospitalizations and improves exercise tolerance and left ventricular function (PROVED and RADIANCE)
    Increased mortality
  89. 89Indications for primary prevention:EF < 35%
    NYHA functional class II or III. Why not class IV patients?
  90. 90Indications:EF < 35%
    QRS > 130 with LBBB or > 150 ms even without LBBB (class II to IV)
  91. 91How does it help?Improves LV systolic function
    Decreases adverse remodeling and dilation of the LV (CARE-HF trial)
  92. 92When to Send Your Patient to the HospitalHypoxia: O2 Sat < 90%
    Respiratory distress
    Acute renal failure
    Worsening symptoms despite increasing diuretic dosing
    Hypotension
    Severe hypokalemia or hyponatremia
  93. 93Advanced Heart TherapiesIntra-aortic balloon pump
    LVAD (left ventricular assist device)
    BiVAD (biventricular assist device)
    Heart transplant
  94. 94Heart TransplantBest mortality data of all advanced heart therapies
  95. 95Patient EducationAvoid salt. More important than fluid restriction.
    Avoid smoking, alcohol, street drugs, obesity.
    If you gain weight suddenly, this could be water weight, and you may need to increase your diuretic. Talk to your doctor.
  96. 96part 1It’s a lot of pills! Adherence, however, does increase the years of your life.
    Refer everyone to cardiac rehab who is willing to do it.
    Home health or phone visits with CHF nurse.
    Goals of care discussions with palliative care referral if necessary.

Informações

Descrição
FlashCards sobre sept 9, criado por Shylla T em 09-09-2020.
Criado por
Shylla T
Visualizações
0
Avaliação

Fale Conosco

Sobre o que é sua mensagem?

O que você acha do novo visual?

Você gostou?