Heart failure
Philip Woodrow in Nursing Acutely Ill Adults, 2015
Heart failure may be acute, chronic, or acute-on-chronic. Acute heart failure typically occurs from acute cardiac events, such as myocardial infarction or severe sepsis. It is sometimes called ‘decompensated’ heart failure, because the failing heart ejects small pulses, while compensatory mechanisms fail to sustain blood pressure. Hypotension usually causes hypoperfusion, progressing to cardiogenic shock (see Chapters 13), usually necessitating transfer to coronary or intensive care units. This chapter focuses primarily on chronic and acute-on-chronic failure, both of which are a major burden on public health, causing and complicating many acute hospital admissions. Acute heart failure is discussed further in the next chapter, although pathophysiology of acute and chronic failure share much in common.
Pharmacological therapy
ILEANA PIÑA, SIDNEY GOLDSTEIN, MARK E DUNLAP in The Year in Heart Failure, 2005
The treatment of acute decompensated heart failure remains of significant interest, as this major public health problem continues to present a major morbidity and mortality burden and economic consequence for patients with heart failure. Knowledge concerning nesiritide, one of the few therapies for acute heart failure supported by randomized clinical trial results, continues to accumulate. Several studies on diverse aspects of this drug continue to testify to its clinical utility. Finally, new data on inotropic agents and a number of investigational pharmaceutical agents are reviewed. Digoxin remains a controversial drug for many, but new data suggest that optimal dosing may help to improve outcomes on this therapy. New results with antagonism of vasopressin and endothelin-1 raise the possibility that inhibition of these neurohormones may produce clinical benefits in patients with heart failure. All of the above work serves to highlight the continued public health and clinical importance of heart failure, a syndrome which still claims too many lives and impairs quality oflife too often. Application of new information reviewed in this section will provide additional strategies for the more effective treatment of this syndrome.
Preoperative Care Including the High-Risk Surgical Patient
Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie in Bailey & Love's Short Practice of Surgery, 2018
Left ventricular failure is the end result of several conditions including IHD, hypertension, cardiomyopathies and valve dysfunction. Decompensated heart failure puts the patient at risk of multiorgan failure. Those with ejection fractions of less than 35%, and in whom the failure is undiagnosed or its severity underestimated, are at the highest risk. The patient’s functional capacity needs to be assessed and surgery may have to be delayed for investigations such as an echocardiogram and/or for optimisation of medical therapy. Drugs used in chronic heart failure have significant implications for perioperative care, and P-blockers and probably ACE inhibitors (unless renal perfusion is to be significantly affected) should be continued. Anaesthesia should ensure minimal myocardial depression and change in afterload during surgery. Arrhythmias must be rapidly brought under control, particularly AF, and correcting any electrolyte imbalance is crucial in this respect. Invasive monitoring of trends in central venous and arterial pressure monitoring may help management, particularly when large fluid shifts are expected to occur.
A giant left atrial myxoma causing mitral valve pseudostenosis – a mimicker
Published in Journal of Community Hospital Internal Medicine Perspectives, 2021
Basel Abdelazeem, Hafiz Khan, Hameem Changezi, Ahmad Munir
CM is a rare condition with an incidence of 0.5 per one million annually [1]. Although it is a benign tumor, it can result in potentially life-threatening conditions. A detailed history and physical examination are crucial for early diagnosis. Cardiovascular symptoms, including chest pain, syncope, dyspnea, and angina, are the most common features in around 67% of the patients, out of which 28% can present with acute decompensated heart failure (ADHF) [4]. Constitutional symptoms, including fever, malaise, arthralgia, and myalgia, are the second most common presentation in around 34%, while the embolic symptoms constitute up to 29% of the patients. Left-sided CM embolizes systemically to cerebral circulation (most common site, up to 30–40% of the patients), kidneys, and lower extremities, while the right-sided CM embolization occurs to pulmonary circulation [5,6]. In an asymptomatic patient, CM can be an incidental finding on imaging.
Association of galectin-3 with changes in left ventricular function in recent-onset dilated cardiomyopathy
Published in Biomarkers, 2019
Andreas J. Rieth, Claudia Jung, Henning Gall, Andreas Rolf, Veselin Mitrovic, Christian W. Hamm, Johannes Sperzel, Christoph Liebetrau
A total of 80 patients with nonischemic DCM (68,8% men; median age 53 years [IQR 48–64]) were included in the analysis. Baseline characteristics are given in Table 1. LVEF was markedly reduced (median 25% [IQR 20–30]), with 76% of patients <35%. Left ventricular remodeling was present in all patients with a median LVEDD of 65 mm [IQR 59–69]. Right ventricular dysfunction, defined as tricuspid annular plain systolic excursion ≤16 mm, was observed in 25 patients (31.25%). Approximately half of all patients studied (48.8%) had a history of acutely decompensated heart failure. Clinical heart failure was present with advanced functional class (NYHA II/III: 72.5%, NYHA IV: 20%) and elevated natriuretic peptides (median NT-proBNP 1978 pg/mL [IQR 817–5587]. Nearly half (48.75%) had a history of acutely decompensated heart failure. The median galectin-3 level was 16.1 ng/mL [IQR 12.0–21.2]. CMR-LGE was present in 45 of 68 patients (66.12%). Almost all patients were on ß-blockers (96.3%) and angiotensin-converting enzyme inhibitors/angiotensin receptor blockers (96.3%) at discharge after primary diagnostics (Table 1).
First Experience with the MitraClip XTR® Compared to the MitraClip NTR® System in a Patient with Severe Mitral Regurgitation and Complex Mitral Valve Anatomy
Published in Structural Heart, 2019
Johannes Patzelt, Rezo Jorbenadze, Markus Renner, Juergen Schreieck, Christian Schlensak, Meinrad Gawaz, Peter Seizer, Harald F. Langer
The patient presented with a history of repeated hospitalization due to decompensated heart failure. Echocardiography showed a good systolic left ventricular (LV) function with severe primary MR with a prolapse of the anterior mitral valve (MV) leaflet (AML) in segment 2 with an eccentric posterior-directed jet (Figure 1A,B). Furthermore, calcifications were present with a restrictive posterior MV leaflet (PML) (Figure 1C). 3D EROA (effective regurgitant orifice area) was measured as 1.46 cm2 (Figure 1D). A decision for PMVR was made by our interdisciplinary heart team due to severe comorbidities. Although in difficult mitral valve anatomies mechanical ventilation with elevated positive end-expiratory pressure may facilitate PMVR,2 we chose to carry out the intervention in conscious sedation considering the frailty of our patient.
Related Knowledge Centers
- Acute Respiratory Distress Syndrome
- Arrhythmia
- Edema
- Fatigue
- Myocardial Infarction
- Shortness of Breath
- Thyroid Disease
- Infection
- Heart Failure
- Shortness of Breath
- Decompensation