Saving Christmas: Use of Analogy to Teach The Compensatory Mechanisms of the Heart in Heart Failure

HAPS Educator ◽  
2018 ◽  
pp. 171-175
Author(s):  
Krista L. Rompolski
Keyword(s):  
Heart Failure ◽  
Compensatory Mechanisms

Investigation of the Relationship Between Color M-Mode Early Diastolic Propagation Velocity and Left Ventricular Adverse Pressure Gradients

2010 ◽  
Author(s):  
Kelley C. Stewart ◽  
Rahul Kumar ◽  
John J. Charonko ◽  
Pavlos P. Vlachos ◽  
William C. Little
Keyword(s):  
Heart Failure ◽  
Diastolic Dysfunction ◽  
Diastolic Heart Failure ◽  
Diagnostic Techniques ◽  
Left Ventricular Diastolic Dysfunction ◽  
Left Ventricular ◽  
Pressure Gradients ◽  
Compensatory Mechanisms ◽  
Ventricular Diastolic Dysfunction ◽  
The Relationship

Left ventricular diastolic dysfunction (LVDD) and diastolic heart failure are conditions that affect the filling dynamics of the heart and affect 36% of patients diagnosed with congestive heart failure [1]. Although this condition is very prevalent, it currently remains difficult to diagnose due to inherent atrio-ventricular compensatory mechanisms including increased heart rate, increased left ventricular (LV) contractility, and increased left atrial pressure (LA). A greater comprehension of the governing flow physics in the left ventricle throughout the introduction of the heart’s compensatory mechanisms has great potential to substantially increase the understanding of the progression of diastolic dysfunction and in turn advance the diagnostic techniques.

Different expression of adrenoceptors and GRKs in the human myocardium depends on heart failure ethiology and correlates to clinical variables

2012 ◽  
Vol 303 (3) ◽  
pp. H368-H376 ◽  
Author(s):  
Fermí Montó ◽  
Eduardo Oliver ◽  
Diana Vicente ◽  
Joaquín Rueda ◽  
Jaime Agüero ◽  
...  
Keyword(s):  
Heart Failure ◽  
Protective Role ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Compensatory Mechanisms ◽  
Human Heart Failure ◽  
Ventricular Ejection Fraction ◽  
Clinical Variables ◽  
G Protein Coupled ◽  
Better Than

Downregulation of β1- adrenergic receptors (β1-ARs) and increased expression/function of G-protein-coupled receptor kinase 2 (GRK2) have been observed in human heart failure, but changes in expression of other ARs and GRKs have not been established. Another unresolved question is the incidence of these compensatory mechanisms depending on heart failure etiology and treatment. To analyze these questions, we quantified the mRNA/protein expressions of six ARs (α1A, α1B, α1D, β1, β2, and β3) and three GRKs (GRK2, GRK3, and GRK5) in left (LV) and right ventricle (RV) from four donors, 10 patients with ischemic cardiomyopathy (IC), 14 patients with dilated cardiomyopathy (DC), and 10 patients with nonischemic, nondilated cardiopathies (NINDC). We correlated the changes in the expressions of ARs and GRKs with clinical variables such as left ventricular ejection fraction (LVEF) and left ventricular end-systolic and left ventricular end-diastolic diameter (LVESD and LVEDD, respectively). The main findings were 1) the expression of the α1A-AR in the LV positively correlates with LVEF; 2) the expression of GRK3 and GRK5 inversely correlates with LVESD and LVEDD, supporting previous observations about a protective role for both kinases in failing hearts; and 3) β1-AR expression is downregulated in the LV and RV of IC, in the LV of DC, and in the RV of NINDC. This difference, better than an increased expression of GRK2 (not observed in IC), determines the lower LVEF in IC and DC vs. NINDC.

scholarly journals Cerebral blood flow changes during intermittent acute hypoxia in patients with heart failure

2018 ◽  
Vol 46 (10) ◽  
pp. 4214-4225 ◽  
Author(s):  
Antonio P. Mansur ◽  
Glaura Souza Alvarenga ◽  
Liliane Kopel ◽  
Marco Antonio Gutierrez ◽  
Fernanda Marciano Consolim-Colombo ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Carotid Artery ◽  
Brachial Artery ◽  
Minute Ventilation ◽  
Acute Hypoxia ◽  
Carbon Dioxide Concentration ◽  
Control Group ◽  
Compensatory Mechanisms

Objective Heart failure (HF) is associated with intermittent hypoxia, and the effects of this hypoxia on the cardiovascular system are not well understood. This study was performed to compare the effects of acute hypoxia (10% oxygen) between patients with and without HF. Methods Fourteen patients with chronic HF and 17 matched control subjects were enrolled. Carotid artery changes were examined during the first period of hypoxia, and brachial artery changes were examined during the second period of hypoxia. Data were collected at baseline and after 2 and 4 minutes of hypoxia. Norepinephrine, epinephrine, dopamine, and renin were measured at baseline and after 4 minutes hypoxia. Results The carotid blood flow, carotid systolic diameter, and carotid diastolic diameter increased and the carotid resistance decreased in patients with HF. Hypoxia did not change the carotid compliance, distensibility, brachial artery blood flow and diameter, or concentrations of sympathomimetic amines in patients with HF, but hypoxia increased the norepinephrine level in the control group. Hypoxia increased minute ventilation and decreased the oxygen saturation and end-tidal carbon dioxide concentration in both groups. Conclusion Hypoxia-induced changes in the carotid artery suggest an intensification of compensatory mechanisms for preservation of cerebral blood flow in patients with HF.

scholarly journals A Clinical Review of Ventricular Arrhythmias in Patients with Congestive Heart Failure

2019 ◽  
Author(s):  
Noel Boyle
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Ventricular Arrhythmias ◽  
Beta Blockers ◽  
Management Strategies ◽  
Significant Risk ◽  
Holter Monitoring ◽  
Current Evidence ◽  
Compensatory Mechanisms ◽  
Ventricular Ejection Fraction

Heart failure is an increasingly prevalent condition, which is associated with ventricular arrhythmias. The reduction in cardiac pumping efficiency leads to the activation of several compensatory mechanisms. These mechanisms eventually lead to cardiac remodelling and a decline in haemodynamic status, contributing to the formation of a substrate conducive to arrhythmias, including increased automaticity, triggered activity, and, most commonly, re-entry circuits. In turn, ventricular arrhythmias can lead to the worsening of heart failure. A diagnosis of heart failure and ventricular arrhythmias is obtained using the patient’s history, examination findings, and investigation results. A key tool in this is echocardiogram imaging, which visualises the cardiac chambers, determines ventricular ejection fraction, and identifies structural abnormalities. A reduction in ejection fraction is a significant risk factor for the development of ventricular arrhythmias. Arrhythmias are diagnosed by ECG, Holter monitoring, and telemetry or event monitoring, and should initially be treated by optimising the medical management of heart failure. Anti-arrhythmic drugs, including beta-blockers, are usually the first-line therapy. Sudden cardiac death is a significant cause of mortality in heart failure patients, and implantable cardioverter defibrillator devices are used in both primary and secondary prevention. Anti-arrhythmic drugs and catheter ablation are important adjunctives for minimising shock therapy. In addition, autonomic modulation may offer a novel method of controlling ventricular arrhythmias. The objective of this review is to provide a practical overview of this rapidly developing field in relation to current evidence regarding the underlying pathophysiology, burden of disease, and management strategies available.

Beginners guide to cardiac pharmacology

2019 ◽  
Vol 10 (4) ◽  
pp. 204-209
Author(s):  
Charlotte Pace
Keyword(s):  
Heart Failure ◽  
Heart Disease ◽  
Adverse Effects ◽  
Mode Of Action ◽  
Cardiac Patients ◽  
Compensatory Mechanisms ◽  
Know How

Drugs used to treat heart disease and heart failure are divided into categories depending on their mode of action. The three main groups are diuretics to remove excess fluid, positive inotropes to improve contractility, and neurohormonal inhibitors that prevent activation of compensatory mechanisms. Drugs used to treat arrhythmias are divided into those that target tachyarrhythmias, and those that act on bradyarrhythmias. All drugs used in cardiac patients can have adverse effects and so it is vital that veterinary nurses know how they work and how to monitor them.

scholarly journals Biomechanical assessment of remote and postinfarction scar remodeling following myocardial infarction

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Mihaela Rusu ◽  
Katrin Hilse ◽  
Alexander Schuh ◽  
Lukas Martin ◽  
Ioana Slabu ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Type I Collagen ◽  
De Novo ◽  
Heart Function ◽  
Type Iii Collagen ◽  
Type I ◽  
Compensatory Mechanisms ◽  
Biomechanical Assessment ◽  
Type V

AbstractThe importance of collagen remodeling following myocardial infarction (MI) is extensively investigated, but little is known on the biomechanical impact of fibrillar collagen on left ventricle post-MI. We aim to identify the significant effects of the biomechanics of types I, III, and V collagen on physio-pathological changes of murine hearts leading to heart failure. Immediately post-MI, heart reduces its function (EF = 40.94 ± 2.12%) while sarcomeres’ dimensions are unchanged. Strikingly, as determined by immunohistochemistry staining, type V collagen fraction significantly grows in remote and scar for sustaining de novo-types I and III collagen fibers’ assembly while hindering their enzymatic degradation. Thereafter, the compensatory heart function (EF = 63.04 ± 3.16%) associates with steady development of types I and III collagen in a stiff remote (12.79 ± 1.09 MPa) and scar (22.40 ± 1.08 MPa). In remote, the soft de novo-type III collagen uncoils preventing further expansion of elongated sarcomeres (2.7 ± 0.3 mm). Once the compensatory mechanisms are surpassed, the increased turnover of stiff type I collagen (>50%) lead to a pseudo-stable biomechanical regime of the heart (≅9 MPa) with reduced EF (50.55 ± 3.25%). These end-characteristics represent the common scenario evidenced in patients suffering from heart failure after MI. Our pre-clinical data advances the understanding of the cause of heart failure induced in patients with extended MI.

The Role of Natriuretic Peptides in the Pathophysiology and Treatment of Heart Failure

2017 ◽  
pp. 1-16
Author(s):  
Jennifer L. Mathews ◽  
Anne Schweighardt
Keyword(s):  
Heart Failure ◽  
Cardiac Output ◽  
Natriuretic Peptide ◽  
Natriuretic Peptides ◽  
Plasma Concentrations ◽  
Compensatory Mechanisms ◽  
Renin Angiotensin ◽  
Sympathetic Nervous Systems ◽  
Ventricular Cells ◽  
Ventricular Filling

The pathophysiology of heart failure is due in part to compensatory mechanisms utilized to maintain cardiac output. Neurohormonal responses include activation of the renin-angiotensin-aldosterone and sympathetic nervous systems leading to vasoconstriction, increased blood volume through reabsorption of sodium and water, and increased myocardial contractility and heart rate. Prolonged activation of these systems often results in a maladaptive response and a further reduction in cardiac output (Colucci, 2015). Natriuretic peptides counterbalance the neurohormonal systems by antagonizing the actions of renin-angiotensin-aldosterone, promoting vasodilation and natriuresis. In hypervolemic states atrial myocytes are stretched resulting in the release of atrial natriuretic peptide (ANP). Ventricular cells secrete brain-type natriuretic peptide (BNP) in response to the high ventricular filling pressures (de Sa, 2008). The natriuretic peptides are degraded enzymatically by neprilysin. Plasma concentrations of ANP and BNP can be used as markers for the diagnosis of heart failure (Grewal, 2004). The kidneys also produce a natriuretic peptide, urodilatin, and new studies suggest a role for this peptide in the pathophysiology and treatment of heart failure (Anker, 2015). The natriuretic peptides can be targeted therapeutically for the treatment of heart failure. Nesiritide, a recombinant preparation of human B-type natriuretic peptide (BNP), is FDA approved and has been available for several years for treatment of acute decompensations of heart failure, but has received limited use due to cost and adverse effect profile. Ularatide, a synthetic analog of urodilatin, is currently in phase three clinical trials. In addition, the FDA has recently approved an angiotensin receptor blocker-neprilysin inhibitor that has shown mortality benefit.

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