Acute cardiac failure: definitions, investigation, and management

2010 ◽  
pp. 2728-2728
Author(s):  
Andrew L Clark ◽  
John G. F Cleland

Presentations of acute heart failure fall into three overlapping categories: (1) acute breathlessness and pulmonary oedema, (2) chronic fluid retention and peripheral oedema (anasarca), and (3) cardiogenic shock. Examination features include tachycardia, hypotension, a raised venous pressure, basal crackles, and peripheral oedema. Auscultation may reveal a third heart sound or features of precipitating valvular heart disease. Initial management focuses on confirming the diagnosis and identification of the immediate precipitant (e.g. arrhythmias, myocardial infarction, decompensating valvular heart disease). Initial investigations include a 12-lead electrocardiogram (ECG), chest radiograph, full blood count, biochemical screen, troponin and thyroid function. Brain natriuretic peptide (BNP) is useful in confirming the diagnosis where clinical features are present and a normal BNP is helpful in excluding the diagnosis. All patients should undergo echocardiographic assessment early in the course of a hospital admission to assess left ventricular function and to look for underlying valvular heart disease. In patients with acute pulmonary oedema investigation and management should proceed simultaneously. Intravenous loop diuretics and nitrates are commonly used therapies and may be combined with ventilatory support with oxygen and continuous positive airways ventilation. Mechanical support may be appropriate as a bridge to definitive therapy in potentially reversible causes. Inotropes are often used but without convincing evidence that they improve outcome. In patients with features are of peripheral oedema and low cardiac output, fluid retention (usually >5 litres) is the predominant feature. Management is principally with bed rest, loop diuretics (usually by intravenous infusion), and, where appropriate, aldosterone antagonists. Thiazide diuretics can be added in resistant cases. Prophylactic low molecular weight heparin should be prescribed. Careful monitoring of fluid balance with daily weights and daily electrolytes is essential. Angiotensin converting enzyme (ACE) inhibitors and subsequently β‎-blockade can be introduced once a satisfactory diuresis has been achieved. Management of cardiogenic shock is usually determined by the cause. Fluid status should be assessed and an adequate left ventricular filling pressure ensured by the administration of intravenous fluids where required (particularly in the case of right ventricular infarction). Revascularization is the mainstay of therapy in acute myocardial infarction. Circulatory support with intra-aortic balloon counter-pulsation (IABP), inotropic agents, ventricular assist devices (VADs), and extracorporeal membrane oxygenation should be considered for reversible causes (e.g. ventricular septal rupture, papillary muscle rupture, acute myocarditis and postpartum cardiomyopathy). Hospital admission with acute heart failure caries a poor prognosis with an average in-hospital mortality of 10–15% rising to up to 60% at 30 days in cases of cardiogenic shock.

2020 ◽  
pp. 3397-3407
Author(s):  
Andrew L. Clark ◽  
John G.F. Cleland

Presentations of acute heart failure fall into three overlapping categories: acute breathlessness and pulmonary oedema; chronic fluid retention and peripheral oedema (anasarca); and cardiogenic shock. Features on examination include tachycardia, hypotension, a raised venous pressure, basal crackles, and peripheral oedema. Auscultation may reveal a third heart sound or features of valvular heart disease. Initial management focuses on confirming the diagnosis and identification of the immediate precipitant (e.g. arrhythmias, myocardial infarction, decompensating valvular heart disease). Initial investigations include a 12-lead electrocardiogram, chest radiograph, full blood count, biochemical screen, troponin, and thyroid function. Natriuretic peptides are useful in confirming the diagnosis where clinical features are present and a normal level of these is helpful in excluding the diagnosis. All patients should undergo echocardiographic assessment early in the course of a hospital admission to assess left ventricular function and to look for underlying valvular heart disease.


2021 ◽  
Vol 10 (18) ◽  
Author(s):  
Linda S. B. Johnson ◽  
Jonas Oldgren ◽  
Tyler W. Barrett ◽  
Candace D. McNaughton ◽  
Jorge A. Wong ◽  
...  

Background Heart failure (HF) is a common complication to atrial fibrillation (AF), leading to rehospitalization and death. Early identification of patients with AF at risk for HF might improve outcomes. We aimed to derive a score to predict 1‐year risk of new‐onset HF after an emergency department (ED) visit with AF. Methods and Results The RE‐LY AF (Randomized Evaluation of Long‐Term Anticoagulant Therapy) registry enrolled patients with AF presenting to an ED in 47 countries, and followed them for a year. The end point was HF hospitalization and/or HF death. Among 15 400 ED patients, 9765 had no prior HF (mean age, 64.9±14.9 years). Within 1 year, new‐onset HF developed in 6.8% of patients, of whom 21% died of HF. Independent predictors of HF included left ventricular hypertrophy (odds ratio [OR], 1.47; 95% CI, 1.19–1.82), valvular heart disease (OR, 1.55; 95% CI, 1.18–2.04), smoking (OR, 1.42; 95% CI, 1.12–1.78), height (OR, 0.93; 95% CI, 0.90–0.95 per 3 cm), age (OR, 1.11; 95% CI, 1.07–1.15 per 5 years), rheumatic heart disease (OR, 1.77, 95% CI, 1.24–2.51), prior myocardial infarction (OR, 1.85; 95% CI, 1.45–2.36), remaining in AF at ED discharge (OR, 1.86; 95% CI, 1.46–2.36), and diabetes (OR, 1.33; 95% CI, 1.09–1.64). A continuous risk prediction score (LVS‐HARMED [left ventricular, valvular heart disease, smoking or other tobacco use, height, age, rheumatic heart disease, myocardial infarction, emergency department discharge rhythm, and diabetes]) had good discrimination (C statistic, 0.735; 95% CI, 0.716–0.755). Validation was conducted internally using bootstrapping (optimism‐corrected C statistic, 0.705) and externally (C statistic, 0.699). The 1‐year incidence of HF hospitalization and/or HF death across quartile groups of the score was 1.1%, 4.5%, 6.9%, and 14.4%, respectively. LVS‐HARMED also predicted incident stroke (C statistic, 0.753; 95% CI, 0.728–0.778). Conclusions The LVS‐HARMED score predicts new‐onset HF after an ED visit for AF. Preventative strategies should be considered in patients with high LVS‐HARMED HF risk.


Author(s):  
Matthew A. Brown ◽  
Farooq H. Sheikh ◽  
Sara Ahmed ◽  
Samer S. Najjar ◽  
Ezequiel J. Molina

Abstract Left ventricular assist devices (LVAD) are increasingly being used as destination therapy in patients with Stage D heart failure. It has been reported that a majority of patients who receive a durable LVAD (dLVAD) present in cardiogenic shock due to decompensated heart failure (ADHF‐CS). As it stands, there is no consensus on the optimal management strategy for patients presenting with ADHF. Bridging with intra‐aortic balloon pumps (IABPs) continues to be a therapeutic option in patients with hemodynamic instability due to cardiogenic shock. The majority of data regarding the use of IABP in cardiogenic shock come from studies in patients presenting with acute myocardial infarction with cardiogenic shock and demonstrates that there is no benefit of routine IABP use in this patient population. However, the role of IABPs as a bridge to dLVAD in ADHF‐CS has yet to be determined. The hemodynamic changes seen in acute myocardial infarction with cardiogenic shock are known to be different and more acutely impaired than those presenting with ADHF‐CS as evidenced by differences in pressure/volume loops. Thus, data should not be extrapolated across these 2 very different disease processes. The aim of this review is to describe results from contemporary studies examining the use of IABPs as a bridge to dLVAD in patients with ADHF‐CS. Retrospective evidence from large registries suggests that the use of IABP as a bridge to dLVAD is feasible and safe when compared with other platforms of temporary mechanical circulatory support. However, there is currently a paucity of high‐quality evidence examining this increasingly important clinical question.


Author(s):  
Luca Baldetti ◽  
Matteo Pagnesi ◽  
Mario Gramegna ◽  
Alessandro Belletti ◽  
Alessandro Beneduce ◽  
...  

Trials on intra-aortic balloon pump (IABP) use in cardiogenic shock related to acute myocardial infarction have shown disappointing results. The role of IABP in cardiogenic shock treatment remains unclear, and new (potentially more potent) mechanical circulatory supports with arguably larger device profile are emerging. A reappraisal of the physiological premises of intra-aortic counterpulsation may underpin the rationale to maintain IABP as a valuable therapeutic option for patients with acute decompensated heart failure and tissue hypoperfusion. Several pathophysiological features differ between myocardial infarction- and acute decompensated heart failure–related hypoperfusion, encompassing cardiogenic shock severity, filling status, systemic vascular resistances rise, and adaptation to chronic (if preexisting) left ventricular dysfunction. IABP combines a more substantial effect on left ventricular afterload with a modest increase in cardiac output and would therefore be most suitable in clinical scenarios characterized by a disproportionate increase in afterload without profound hemodynamic compromise. The acute decompensated heart failure syndrome is characterized by exquisite afterload-sensitivity of cardiac output and may be an ideal setting for counterpulsation. Several hemodynamic variables have been shown to predict response to IABP within this scenario, potentially guiding appropriate patient selection. Finally, acute decompensated heart failure with hypoperfusion may frequently represent an end stage in the heart failure history: IABP may provide sufficient hemodynamic support and prompt end-organ function recovery in view of more definitive heart replacement therapies while preserving ambulation when used with a transaxillary approach.


2021 ◽  
pp. 78-81
Author(s):  
Somil Verma ◽  
Mahendra Pratap ◽  
S.L Mathur

BACKGROUND- Acute myocardial infarction (AMI) remains a major cause of morbidity and mortality worldwide. Initial evidence suggests that Procalcitonin (PCT) can act as a potential blood based biomarker in AMI. Therefore, it may be helpful in prognostication and risk-stratication of patients with STelevation myocardial infarction (STEMI) and help us to predict the risk of cardiovascular complications and outcome. AIM- To study the association of PCTlevels at the time of admission with incidence of cardiovascular complications in terms of cardiogenic shock, heart failure, arrhythmia and death in patients admitted with STEMI. METHOD- Aprospective observational study was conducted in a tertiary care centre of India. Patients diagnosed with STEMI were enrolled in the study after making the necessary exclusions. The PCT levels were checked at the time of admission along with electrocardiography (ECG), Echocardiography, Troponin I ,total leukocyte count (TLC), blood urea, creatinine and liver function test (LFT). Patients were followed till discharge / death and outcomes were recorded. RESULT- Two hundred and fty patients were included in the study (57.60 % males, mean age- 59.77±13.63 years). High PCT levels (>0.10 ng/ml) were signicantly associated with cardiovascular complications in terms of cardiogenic shock, arrhythmia's, heart failure and signicant left ventricular dysfunction. Raised PCTlevel was found to be a good predictor of mortality (relative risk =10.51). CONCLUSION- Raised PCT levels were associated with higher cardiovascular complications and mortality in patients with STEMI. PCT levels at the time of admission may be useful as a biomarker in prognostication and risk stratication of STEMI patients.


2021 ◽  
Vol 10 (7) ◽  
pp. 409-413
Author(s):  
Shivakumar B.G. ◽  
Shivakumar N ◽  
Siddharth Gosavi ◽  
Shashank Shastry

BACKGROUND The study was conducted in an attempt to correlate serum uric acid levels with Killip class i.e. severity of heart failure in patients with acute myocardial infarction and to assess any influence of serum uric acid levels on predicting prognosis in patients with acute myocardial infarction. Ischaemic heart disease, particularly acute myocardial infarction is one of the leading causes of death across the world accounting for 12.7 % of global mortality. Low and middle-income countries are facing 80 % of the global burden of ischaemic heart disease death. Since the pathophysiology of acute myocardial infarction is complicated, proper risk stratification is essential for appropriate management and better outcome. Serum uric acid levels (SUA) have been correlated with coronary artery calcification and atherosclerosis. High SUA levels also have been identified as a risk marker for cardiovascular disease development, progression and mortality. METHODS The study design was a one-year cross-sectional study. 100 patients admitted with acute myocardial infarction within one day of the start of symptoms in the Department of Cardiology & Medicine were included from September 2018 to September 2019. In this study, patients with known causes of elevated uric acid levels (chronic kidney disease, gout, haematological malignancy, hypothyroidism, metabolic syndrome, myeloproliferative disease, lymphoproliferative disease, drugs– pyrazinamide, diuretics, ethambutol, ethanol, malignancy, G6PD deficiency and psoriasis) were included. Patients on drugs which raise serum uric acid e.g., salicylates (2 gm / d, hydrochlorothiazide, pyrazinamide), and chronic alcoholics were not included. Patients were further subjected to investigations like serum uric acid, ECG, 2D echo and other routine investigations. Urine albumin levels, troponin I, chest x-ray, fundoscopy, and fasting lipid profile were done. Investigation reports were analysed with the clinical profile and the data was compiled and appropriate statistical test was applied. RESULTS There were more cases of myocardial infarction above 40 years as compared to below 40 years of age and males (69 %) were more as compared to females (31 %) with the commonest presentation as chest pain. Majority of the patients had inferior wall myocardial infarction (IWMI) (40 %) and most (91 %) of the patients had left ventricular (LV) dysfunction (mild, moderate and severe). More patients with Killip class III and IV had abnormal uric acid levels as compared to class I, and II. Among 27 patients who expired, 23 were in Killip class III and IV (13 in Killip class III and 10 in class IV) and the mean serum uric acid levels of expired patients were elevated on all the 3 days with maximum elevation on day 1. CONCLUSIONS Patients with higher Killip class had higher levels of serum uric acid in comparison to patients of lower Killip class. Serum uric acid level in association with Killip class is a good predictor of the severity of heart failure and short-term mortality after myocardial infarction.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Hideki Okui ◽  
Shuichi Hamasaki ◽  
Sanemasa Ishida ◽  
Masakazu Ogawa ◽  
Keishi Saihara ◽  
...  

Background: The coronary microvascular vasodilating function is an important determinant of patient outcomes in a number of clinical settings, including coronary artery disease, hypertensive heart disease, or cardiomyopathy. However, the characteristics or the implication of coronary microcirculation in valvular heart disease has not been fully elucidated. The present study was designed to assess coronary vasodilating function and its effects on systolic function in patients with aortic regurgitation (AR) and mitral regurgitation (MR). Methods: Forty-four consecutive patients (66 yrs) with moderate to severe AR and 45 consecutive patients with moderate to severe MR (64 yrs) were enrolled for this study. All patients were free of coronary artery stenosis. Fifty-one age-matched patients without underlying cardiovascular disease served as controls. Endothelium-dependent and endothelium-independent vasodilating function of resistance coronary artery were assessed by coronary blood flow (CBF) response to acetylcholine and papaverine, respectively. Left ventricular ejection fraction (LVEF) was determined by echocardiography as an indicator of systolic function. Results: In patients with AR, both %change in CBF response to acetylcholine and papaverine were significantly lower than controls (32 ± 61 vs 64 ± 84, 172 ± 87 vs 268 ± 105, p < 0.05, p < 0.01, respectively). Further, %change in CBF response to acetylcholine positively correlated with LVEF (r = 0.45, p < 0.01). In patients with MR, %change in CBF response to papaverine was significantly lower than controls (221 ± 123 vs 268 ± 105, p < 0.05), but %change in CBF response to acetylcholine was comparable with controls. Moreover, neither %change in CBF response to acetylcholine nor CBF response to papaverine had significant correlation with LVEF. Conclusion: In patients with AR, both endothelium-dependent and endothelium-independent vasodilating function of resistance coronary artery were deteriorated. Further, endothelium-dependent vasodilating function may be associated with left ventricular systolic function. Our findings indicate coronary microvascular endothelial dysfunction as a potential target for prevention of systolic heart failure in patients with AR.


2017 ◽  
Vol 24 (06) ◽  
pp. 912-918
Author(s):  
Naeem-ur- Rehman Mir ◽  
Naeem Asghar ◽  
Shaukat Javed

Introduction: Atrial fibrillation (AF) and wider QRS duration have long beenidentified to worsen heart failure and LV dysfunction and increase cardiovascular morbidityand mortality. Therefore, it is necessary to identify those patients of heart failure who are atgreater risk for cardiovascular morbidity and mortality so that such subjects may be focusedfor preventive strategies. An association exists between QRS duration and AF with greaterincidences of cardiovascular events in patients of heart failure with LV systolic dysfunction.Study Design: Cross sectional survey. Setting: Department of Cardiology, Punjab Institute ofCardiology Lahore. Period: 16-02-2015 to 15-08-2015. Material and Methods: The objectiveof study was to determine the Frequency of QRS Duration groups and Atrial Fibrillation inPatients with Left Ventricular Dysfunction. Sample size of 400 cases was calculated with 95%confidence level, 4% margin of error and taking expected percentage of atrial fibrillation innarrow QRS group i.e. 20.9% (least among all) in patients with left ventricular dysfunction.Sampling technique was non-probability, purposive sampling. Result: The study populationconsisted of male (72.3%) and female (27.7%). Mean LA diameter was 40.3±6.08 mm andmean LV ejection fraction 31.8±6.6 % in the study population. Ischemic heart disease wasthe most common cause of LV dysfunction (88.3%) followed by non-ischemic cardiomyopathy(8.75%) and non-Ischemic valvular heart disease (3.5%). The frequency of Narrow QRSd (<120ms) was 62%, Intermediate QRSd (120-150 ms) was 26.5% and Wide QRSd (>150 ms) was11.5%. The frequency of atrial fibrillation in study population was 15.75%. The frequency of atrialfibrillation was highest in Wide QRSd group (>150 ms) i.e. (60.9%), followed by IntermediateQRSd group (120-150 ms) i.e. (18.9%) and narrow QRSd group (<120 ms) i.e. (6.04%). Patientwith atrial fibrillation were more likely to have poor ejection fraction (P<0.0023) and wider QRSduration (P<0.0001). Frequency of atrial fibrillation was highest in Valvular Cardiomyopathy(non-ischemic valvular heart disease) patients (42.8%) as compared to coronary artery diseasegroup (15.3%) and non-ischemic cardimyopathy group (9.4%). Conclusion: In patients of heartfailure with reduced ejection fraction (HFrEF), the frequency of atrial fibrillation increases asQRS duration widens. This group of patients must be focused for AF preventive strategies.


Author(s):  
Brian P Halliday ◽  
Roxy Senior ◽  
Dudley J Pennell

Abstract The measurement of left ventricular ejection fraction (LVEF) is a ubiquitous component of imaging studies used to evaluate patients with cardiac conditions and acts as an arbiter for many management decisions. This follows early trials investigating heart failure therapies which used a binary LVEF cut-off to select patients with the worst prognosis, who may gain the most benefit. Forty years on, the cardiac disease landscape has changed. Left ventricular ejection fraction is now a poor indicator of prognosis for many heart failure patients; specifically, for the half of patients with heart failure and truly preserved ejection fraction (HF-PEF). It is also recognized that LVEF may remain normal amongst patients with valvular heart disease who have significant myocardial dysfunction. This emphasizes the importance of the interaction between LVEF and left ventricular geometry. Guidelines based on LVEF may therefore miss a proportion of patients who would benefit from early intervention to prevent further myocardial decompensation and future adverse outcomes. The assessment of myocardial strain, or intrinsic deformation, holds promise to improve these issues. The measurement of global longitudinal strain (GLS) has consistently been shown to improve the risk stratification of patients with heart failure and identify patients with valvular heart disease who have myocardial decompensation despite preserved LVEF and an increased risk of adverse outcomes. To complete the integration of GLS into routine clinical practice, further studies are required to confirm that such approaches improve therapy selection and accordingly, the outcome for patients.


2020 ◽  
pp. 088506662091877
Author(s):  
Jacob C. Jentzer ◽  
Bradley Ternus ◽  
Mackram Eleid ◽  
Charanjit Rihal

Structural heart disease (SHD) emergencies include acute deterioration of a stable lesion or development of a new critical lesion. Structural heart disease emergencies can produce heart failure and cardiogenic shock despite preserved systolic function that may not respond to standard medical therapy and typically necessitate surgical or percutaneous intervention. Comprehensive Doppler echocardiography is the initial diagnostic modality of choice to determine the cause and severity of the underlying SHD lesion. Patients with chronic SHD lesions which deteriorate due to intercurrent illness (eg, infection or arrhythmia) may not require urgent intervention, whereas patients with an acute SHD lesion often require definitive therapy. Medical stabilization prior to definitive intervention differs substantially between stenotic lesions (aortic stenosis, mitral stenosis, left ventricular outflow tract obstruction) and regurgitant lesions (aortic regurgitation, mitral regurgitation, ventricular septal defect). Patients with regurgitant lesions typically require aggressive afterload reduction and inotropic support, whereas patients with stenotic lesions may paradoxically require β-blockade and vasoconstrictors. Emergent cardiac surgery for patients with decompensated heart failure or cardiogenic shock carries a substantial mortality risk but may be necessary for patients who are not eligible for catheter-based percutaneous SHD intervention. This review explores initial medical stabilization and subsequent definitive therapy for patients with SHD emergencies.


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