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Diagnosis and management of acute heart failure

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Acute heart failure.....pathophysiology and management

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Diagnosis and management of acute heart failure

  1. 1. Alaa Ateya Mohammed
  2. 2. Terms have been used to characterize AHF in the literature, including:  “acute heart failure syndromes” (AHFSs),  “acute(ly) decompensated heart failure” (ADHF),  “acute decompensation of chronic heart failure” (ADCHF),  “hospitalization for heart failure” (HHF).
  3. 3. Acute Heart failure Definition:  AHF can be defined as: “ The new onset or recurrence of symptoms and signs of heart failure requiring urgent or emergent therapy and resulting in seeking unscheduled care or hospitalization.”  Although the designation “acute” in the nomenclature suggests a sudden onset of symptoms, many patients may have a more subacute course, with gradual worsening of symptoms that ultimately reach a level of severity sufficient to seek unscheduled medical care.
  4. 4. Scope of the Problem  The overall number of hospitalizations for heart failure continues to grow as a consequence of: Aging of the population, Improved survival after acute MI, Effective prevention of SCD.
  5. 5. Preserved vs Reduced Ejection Fraction  Unexpectedly high prevalence of HFpEF in AHF  HFpEF are more likely to be older, to be female, and to have a history of hypertension, less likely underlying CAD  The in-hospital mortality for patients with HFpEF appears to be lower than that for patients with depressed LV ejection fraction (LVEF), but postdischarge rehospitalization rates are similarly high for both groups.
  6. 6. Comorbid Conditions with AHF Very common represent diseases that are risk factors for the development of heart failure and also can complicate diagnosis and management.  Hypertension is the most prevalent 60%  CAD 50%  Dyslipidemia > 30%  Diabetes mellitus  Other conditions that are the result of the vascular injury produced by these diseases, such as Stroke, PVD, CKD  COPD 30%(confounds the presenting symptoms dyspnea)  Atrial fibrillation 30-40% (can both precipitate AHF and complicate its management)
  7. 7. PATHOPHYSIOLOGY clinical signs and symptoms ( congestion or end- organ dysfunction, or both) Amplifying mechanisms initiating mechanisms or Triggers underlying substrate
  8. 8. Underlying Substrate  may be one of 1. In most patients with AHF, the original substrate is one of chronic compensated heart failure, followed by decompensation with development of AHF. 2. No previous history of heart failure but exhibit an abnormal substrate (e.g., those with stage B heart failure associated with asymptomatic LV dysfunction) with a first presentation of heart failure (de novo heart failure) 3. No previous history of heart failure in whom AHF develops because of sudden changes in ventricular function from an acute insult such as myocardial infarction or acute myocarditis.
  9. 9. Initiating mechanisms vary according to, and interact with, the underlying substrate Maybe cardiac or extracardiac. For patients with normal substrate (normal myocardium), a substantial insult to cardiac performance (e.g., acute MI, myocarditis) is required to lead to the clinical presentation of AHF. For patients with abnormal substrate at baseline (e.g., asymptomatic LV dysfunction), smaller perturbations (e.g., poorly controlled hypertension, atrial fibrillation, or ischemia) may precipitate an AHF episode. For patients with a substrate of compensated or stable chronic heart failure, medical or dietary noncompliance, drugs such as nonsteroidal anti-inflammatory agents or thiazolidinediones, and infectious processes all are common triggers for decompensation.
  10. 10. “Amplifying Mechanisms”  These include:  Neurohormonal and inflammatory activation,  Ongoing myocardial injury with progressive myocardial dysfunction,  Worsening renal function,  Interactions with the peripheral vasculature “all of which may contribute to the propagation and worsening of the AHF episode”
  11. 11. Congestion  Systemic or pulmonary congestion, most often the result of a high LV diastolic pressure, dominates the clinical presentation in most patients hospitalized for AHF  Gradual increases in intravascular volume lead to symptoms of congestion and clinical presentation, and normalization of volume status with diuretic therapy results in restoration of homeostasis. Although this mechanism may be operative in some patients (particularly those with frank noncompliance with sodium restriction or diuretic therapy), this is “oversimplification”.
  12. 12. Increasing interest in the concept of volume redistribution rather than volume retention as a mechanism of decompensation in heart failure Clinical congestion and hemodynamic congestion  Although patients present with signs and symptoms of systemic congestion such as dyspnea, rales, elevated jugular venous pressure, and edema, this state often is preceded by so-called hemodynamic congestion, defined as high LV diastolic pressures without overt clinical signs.  Similarly, clinical congestion may resolve with treatment but hemodynamic congestion may persist, leading to a high risk of rehospitalization.
  13. 13. hemodynamic congestion may contribute to the progression of heart failure because it may result in:  Wall stress,  (RAAS) and sympathetic nervous system (SNS) activation.  Myocyte loss and increased fibrosis.  Abnormal processing of the natriuretic peptides  Elevated diastolic filling pressures may decrease coronary perfusion pressure, resulting in subendocardial ischemia with further exacerbation of cardiac dysfunction.  Increased LV filling pressures also can lead to a more spherical shape, contributing to worsening mitral regurgitation.  Pathologic remodeling
  14. 14. Myocardial Function  Although a variety of extracardiac factors play important roles in AHF, impairments of cardiac function (systolic, diastolic, or both) remain central to our understanding of this disorder.  Changes in systolic function and decreased arterial filling can initiate a cascade of effects that are adaptive in the short term but maladaptive when elevated chronically, including stimulation of the SNS and the RAA. (vasoconstriction, sodium and water retention, increase and redistribution from other vascular beds, increases in diastolic filling pressures)
  15. 15.  In patients with underlying CAD, initial defects in systolic function may initiate a vicious circle of decreasing coronary perfusion, increased myocardial wall stress, and progressively worsening cardiac performance. Increased LV filling pressures and changes in LV geometry can worsen functional mitral regurgitation, further decreasing cardiac output.
  16. 16.  Approximately half of patients with AHF have relatively preserved systolic function.  Of importance, abnormalities in diastolic function are present in patients with both preserved and impaired ejection fraction.  The impairment of the diastolic phase may be related to passive stiffness or abnormal active relaxation of the left ventricle, or both.  Hypertension, tachycardia, and myocardial ischemia can further impair diastolic filling. All of these mechanisms contribute to higher LV end-diastolic pressures, which are reflected back to the pulmonary capillary circulation.  Diastolic dysfunction alone may be insufficient to lead to AHF, but it serves as the substrate on which other precipitating factors (such as atrial fibrillation, coronary artery disease, or hypertension) lead to decompensation.
  17. 17.  The availability of sensitive assays for circulating cardiac troponins has led to substantial evolution of our understanding of the role of myocardial injury in the pathophysiology of heart failure.  Circulating cardiac troponins are elevated in a large proportion of patients with AHF, even in the absence of clinically overt myocardial ischemia.  30% had persistent elevation of troponin at 30 days  Associated with increased risk of both in-hospital and postdischarge events
  18. 18. The precise mechanisms mediating myocardial injury in AHF are poorly defined:  Increased myocardial wall stress,  Increased myocardial oxygen demand,  Decreased coronary perfusion pressure,  endothelial dysfunction,  Activation of the neurohormonal and inflammatory axes,  Activation of platelets,  Altered calcium handling. All may contribute to myocyte injury even in absence of CAD Specific therapeutic interventions that may increase myocardial oxygen demand (such as positive inotropic agents) or decrease coronary artery perfusion pressure (such as some vasodilators) may exacerbate myocardial injury and further contribute to the cycle of decompensation.
  19. 19. Renal Mechanisms  The kidney plays two fundamental roles relative to the pathophysiology of heart failure: 1) Modulates loading conditions of the heart by controlling intravascular volume 2) Responsible for neurohormonal outputs (i.e., the RAAS system)  Baseline measures of renal function also are well-established risk factors for poor outcomes in AHF  Additionally, worsening renal function during AHF therapy in the setting of persistent congestion—often termed the “cardiorenal syndrome”—has been associated with poor outcomes  Although often assumed to be related to low cardiac output and renal blood flow, careful hemodynamic studies have confirmed that: “The strongest predictor of worsening renal function in heart failure patients relates to elevated central venous pressure, which is reflected back to the renal veins and leads directly to changes in glomerular filtration rate.”
  20. 20.  Diuretics may exacerbate renal dysfunction through increasing neurohormonal activation and vasoconstriction, although in many cases effective diuresis improves renal function by decreasing central venous pressure.  Newer biomarkers that may distinguish changes in renal function (as reflected by serum creatinine or cystatin C) from acute kidney injury (as reflected by markers such as urinary neutrophil gelatinase– associated lipocalin [NGAL]) may allow better differentiation of worsening renal function during AHF hospitalization
  21. 21. Vascular Mechanisms  Increasing appreciation for the importance of the vasculature not only as an underlying cause of cardiac dysfunction (i.e., atherosclerosis, hypertension) but also as a central component of the pathogenesis of AHF  Abnormalities of endothelial function related to nitric oxide– dependent regulation of vascular tone  Arterial stiffness  Peripheral vasoconstriction in the setting of AHF redistributes blood centrally, increasing pulmonary venous congestion and edema.  This increased afterload causes greater ventricular wall stress and increased myocardial ischemia and cardiac arrhythmias  Effects of this vascular abnormality are amplified by LV diastolic dysfunction.
  22. 22. Neurohormonal and Inflammatory Mechanisms  Increased plasma concentrations of norepinephrine, plasma renin activity, aldosterone, and endothelin-1 have been reported in patients with AHF; all of these axes are associated with vasoconstriction and volume retention, which could contribute to myocardial ischemia and congestion, thereby exacerbating cardiac decompensation.  Proinflammatory cytokines such as tumor necrosis factoralpha and interleukin-6 are elevated in patients with AHF  direct negative inotropic effects on the myocardium as well as increasing capillary permeability and inducing endothelial dysfunction.  Stimulates the release of the potent procoagulant tissue factor and endothelin-1, which can lead to further myocardial suppression, disruption of the pulmonary alveolar-capillary barrier, and increased platelet aggregation and coagulation (potentially worsening ischemia)
  23. 23. AHF Groups 1. Decompensated heart failure:  This group is composed of patients with worsening signs and symptoms of congestion on a background of chronic heart failure.  may be acute, subacute, or indolent, with gradually worsening symptoms over days to weeks.  Either preserved or reduced ejection fraction, but cardiac output generally is preserved and blood pressure is within the normal range.  Overall, this group represents the largest proportion of patients hospitalized for AHF.
  24. 24.  2. Acute hypertensive heart failure: Hypertension is increasingly recognized as a common feature of the AHF presentation, with 50% of patients presenting with systolic blood pressure (SBP) higher than 140 mm Hg and 25% with SBP higher than 160 mm Hg.  hypertension may be triggered by a high sympathetic tone related to dyspnea and accompanying anxiety (reactive hypertension)  OR acute hypertension with accompanying changes in afterload may be a trigger for decompensation. Both of these mechanisms may be operative in a given patient,  cause-and-effect relationships may be difficult to discern with precision  patients in whom acute hypertensive heart failure are more likely to have preserved systolic function  Sudden onset of symptoms  Frank pulmonary edema with evident rales and florid congestion on the chest radiograph is much more common in this group of patients than in those with more gradual onset of symptoms, probably related to differences in LV compliance, acuity of pressure changes, and pulmonary lymphatic capacity.
  25. 25. 3. Cardiogenic shock:  This group presents with signs and symptoms of organ hypoperfusion despite adequate preload  SBP often (although not always) is decreased, and evidence of frank or impending end-organ dysfunction (renal, hepatic, central nervous system) is common.  This type of AHF is relatively uncommon (4% )
  26. 26.  Less common AHF clinical scenarios as: isolated right-sided heart failure  high-output heart failure
  27. 27. AHF Clinical Triggers: In the OPTIMIZE-HF registry, 61% of enrolled subjects had an identifiable clinical precipitant:  Pulmonary processes  Myocardial ischemia  Arrhythmias (e.g. AF)  Worsening renal function was responsible for the highest in- hospital mortality rate (8%),  Nonadherence to diet or medication OR Uncontrolled HTN was associated with a much better prognosis (<2% in-hospital mortality for each).  Others: Thyroid disease, Anemeia  More than one precipitant was identified in a substantial minority of the study population.
  28. 28. Biomarkers  The natriuretic peptides are a family of important counterregulatory hormones in heart failure with vasodilatory and other effects  In AHF, both brain natriuretic peptide (BNP) and N-terminal pro–brain natriuretic peptide (NT-proBNP) have an important role in the differential diagnosis in patients presenting in the emergency department with dyspnea  BNP threshold of 100 pg/mL maximized sensitivity and specificity to differentiate dyspnea that ultimately confirmed to be due to AHF:  the negative predictive value of a BNP level less than 100 pg/mL was particularly high (89%),  the positive predictive value of this threshold was (79%)  NT-proBNP has similar diagnostic value, although the appropriate cut points are higher overall and vary with age  False positives (e.g., caused by myocardial infarction or pulmonary embolism)  False negatives (primarily caused by obesity, which results in lower NP levels for a given degree of heart failure)  Natriuretic peptide levels tend to be lower in patients with HFpEF than those with reduced systolic function
  29. 29. D.D. Non-Cardiogenic Pulmonary Edema
  30. 30. MANAGEMENT OF THE PATIENT WITH ACUTE HEART FAILURE  Establish the diagnosis,  Treat life-threatening abnormalities,  Initiate therapies to rapidly provide symptom relief,  Identify the cause and precipitating triggers.
  31. 31. General Approaches to Therapy of Acute Heart Failure Targeting Congestion  The current general approach focuses on the successful treatment of clinical and hemodynamic congestion, while limiting effects on myocardial or end-organ function, identifying addressable triggers, and optimizing proven long-term therapies  Incorporates information from three main aspects of the patient’s clinical presentation: blood pressure, volume status, and renal function
  32. 32. 1) Blood Pressure  Most patients present with elevated blood pressures and consequently will benefit from and safely tolerate vasodilator therapy.  Vasodilators may decrease preload by reversing venous vasoconstriction and the related central volume redistribution from the peripheral and splanchnic venous systems, and reduce afterload by decreasing arterial vasoconstriction with a resultant improvement in cardiac and renal function.
  33. 33.  Hypotension (SBP below 85 to 90 mm Hg) is a poor prognostic sign in patients with AHF.  Asymptomatic hypotension, as an isolated finding in the absence of congestion and poor peripheral or central perfusion, does not require emergent treatment.  Inotropic therapy may be indicated for persistent symptomatic hypotension or evidence of hypoperfusion in the setting of advanced systolic dysfunction.  In general, the use of vasoconstrictors, such as highdose dopamine, phenylephrine, epinephrine, and norepinephrine, should be avoided unless such agents are absolutely necessary for management of refractory symptomatic hypotension or hypoperfusion
  34. 34. 2) Volume Status  Most patients with AHF have evidence of volume overload  Intravenous diuretics remain the foundation of AHF therapy.  Patients with clinically evident congestion typically have 4 to 5 liters of excess volume, and amounts greater than 10 L are not uncommon.  The choice of diuretic regimen is influenced by the amount and rapidity of the desired fluid removal and the renal function.
  35. 35.  Diuresis addresses the underlying abnormality and frequently alleviates symptoms and signs of elevated filling pressures.  However, intravenous vasodilator therapy may provide more rapid relief in highly symptomatic patients with evidence of pulmonary congestion. In fact, many patients with hypertensive AHF may require minimal diuretics.  Careful attention to volume status is critical, because patients’ symptoms of congestion may resolve despite persistent hemodynamic congestion (i.e., elevated filling pressures).  Hospital discharge before hemodynamic congestion is fully treated appears to be a common cause of rehospitalization
  36. 36. 3) Renal Function  Approximately two thirds of patients present with at least moderate renal insufficiency.  This deficit may reflect preexisting kidney disease or may be a manifestation of the worsening heart failure.  Abnormal renal function typically is associated with some degree of diuretic resistance, and higher doses of diuretics or other strategies may be needed.  The important clinical problem of worsening renal function during AHF therapy, the cardiorenal syndrome
  37. 37. Diuretics  Loop diuretics are the primary pharmacologic agents for treatment  of volume overload in patients with AHF  Rapid symptom relief in most patients  This group of agents (furosemide, torsemide, bumetanide, and ethacrynic acid)  intravenous administration avoids variable bioavailability and allows for rapid onset of action (typically within 30 to 60 minutes)  Based on the results of the DOSE study, initial doses of approximately 2.5 times the outpatient dose should be considered for patients on chronic oral diuretic therapy, with underlying renal dysfunction, or with severe volume overload.  Titration should be rapid with doubling of the dose until an effective response is noted.  With significant volume overload (>5 to 10 liters) or diuretic resistance, a continuous intravenous infusion can be considered.
  38. 38. Vasodilators  In the absence of hypotension, vasodilators can be used as first-line agents in combination with diuretics in the management of patients with AHF to improve congestive symptoms  Include the organic nitrates (nitroglycerin [NTG] and isosorbide dinitrate), sodium nitroprusside (SNP), and nesiritide.  All of these drugs act by activating soluble guanylate cyclase (sGC) in the smooth muscle cells, leading to higher intracellular concentrations of cyclic guanosine monophosphate (cGMP) and consequent vessel relaxation  used with caution in patients who are preload- or afterload-dependent (e.g., severe diastolic dysfunction, aortic stenosis, coronary artery disease), because they may cause severe hypotension.  Blood pressure (BP) should be monitored frequently and the drug discontinued if symptomatic hypotension develops.
  39. 39. Nitrates  Organic nitrates are one of the oldest therapeutic agents for management of AHF.  These agents are potent venodilators, producing rapid decreases in pulmonary venous and ventricular filling pressures and improvement in pulmonary congestion, dyspnea, and myocardial oxygen demand at low doses  At slightly higher doses and in the presence of vasoconstriction, nitrates also are arteriolar vasodilators, reducing afterload and increasing cardiac output
  40. 40.  Nitrates are relatively selective for epicardial, compared to intramyocardial, coronary arteries, resulting in increased coronary blood flow and making them useful for patients with concomitant active myocardial ischemia.  Organic nitrates may also be administered orally, sublingually, or by spray, allowing for convenient emergent treatment before establishing intravenous access  The dose may initially be titrated to the goal of immediate symptom relief, but a blood pressure reduction of at least 10 mm Hg in mean arterial pressure with a SBP greater than 100 mm Hg may be preferable.  The nitrate dose may need to be reduced if SBP is 90 to 100 mmHg and often will need to be discontinued with SBP below 90 mm Hg.
  41. 41.  Limitations of organic nitrates: Tolerance that typically develops within 24 hours  Headache is the most common adverse effect (20%) Symptomatic hypotension (5%) but generally resolves when nitrate therapy is discontinued.  In view of the risk of severe hypotension with potentially catastrophic consequences, the recent use of phosphodiesterase-5 inhibitors (sildenafil, tadalafil, and vardenafil) should be ruled out before administration of nitrates
  42. 42. Oxygen  In patients with severe hypoxemia (oxygen saturation [SaO2] <90%), oxygen administration is recommended.  Although oxygen saturation on presentation is inversely related to short-term mortality, inhaled oxygen (FiO2 ≥0.4) may cause detrimental hemodynamic effects (such as hyperoxia-induced vasoconstriction) in patients with systolic dysfunction, so it is not routinely recommended for patients without hypoxemia.  In patients with obstructive pulmonary disease, high concentrations of inhaled oxygen should not be used, to avoid the risk of respiratory depression and worsening hypercarbia.
  43. 43. (NIPPV) & (CPAP)  Noninvasive ventilation (NIV) with continuous positive airway pressure(CPAP) or noninvasive intermittent positive-pressure ventilation(NIPPV) was associated with greater improvement in patient- reported dyspnea, heart rate, acidosis, and hypercapnea after 1 hour of therapy,  although it was not associated with a 7-day mortality benefit or with decreased need for intubation when compared with standard oxygen therapy.
  44. 44. CPAP CPAP typically is initiated with a positive end-expiratory pressure (PEEP) of 5 to 7.5 cm H2O, titrated to 10 cm H2O as needed for dyspnea relief and improvement in O2 saturation.  Contraindications:  immediate need for endotracheal intubation (inability to protect the airway, life-threatening hypoxia)  lack of patient cooperation (altered sensorium, unconsciousness, anxiety, inability to tolerate mask)  Caution is indicated in patients with :  Cardiogenic shock, RV failure, and  Severe obstructive airway disease.  Potential side effects and complications  anxiety, claustrophobia, dry mucous membranes,  worsening RV failure, hypercapnea, pneumothorax, and aspiration
  45. 45.  Morphine may be useful in patients with severe anxiety or distress but should be used cautiously or avoided, especially in the presence of hypotension, bradycardia, advanced atrioventricular block, or CO2 retention.  Morphine use has been associated with increased likelihood of mechanical ventilation, requirement for intensive care unit (ICU) admission, prolonged hospital stay, and death
  46. 46. Thanks for your attention

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