Pathophysiological Mechanisms leading to Heart Failure Essay
Requirements: A 64-year-old woman presents to the primary care office with shortness of breath, leg swelling, and fatigue. She has a history of type 2 diabetes and hypertension. She reports that recently she had been able to go for daily walks with her friends, but in the past month, the walks have become more difficult due to shortness of breath and fatigue. She also sometimes awakens in the middle of the night due to shortness of breath and has to prop herself up on three pillows. On physical examination, she is tachycardic (110 beats per minute) and has a blood pressure of 106/74 mm Hg. Fine crackles are noted on inspiration in bilateral bases. The cardiac exam reveals the presence of a third and fourth heart sound and jugular venous distension. 2+ pitting edema is noted in the knees bilaterally. An ECG shows sinus rhythm at 110 bpm with Q waves in the anterior leads. An echocardiogram shows decreased wall motion of the anterior wall of the heart and an estimated ejection fraction of 25%. Pathophysiological Mechanisms leading to Heart Failure Essay. She is diagnosed with systolic heart failure, secondary to a silent MI. Discuss the pathophysiological mechanisms that can lead to heart failure. Differentiate between systolic and diastolic heart dysfunction Discuss the causes of the patient’s shortness of breath, awakening in the middle of the night and the need to prop herself up on three pillows. Include pathophysiological mechanisms that causes each of these signs and symptoms. Include two points of teaching for this patient Support your response with at least one current evidence based resource.
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Heart failure syndrome is defined as the inability of the heart to deliver adequate blood to the body to meet end-organ metabolic needs and oxygenation at rest or during mild exercise. Myocardial dysfunction can be defined as systolic and/or diastolic, acute or chronic, compensated or uncompensated, or uni- or biventricular. Several counterregulatory mechanisms are activated depending on the duration of the heart failure. Neurohormonal reflexes such as sympathetic adrenergic system, renin-angiotensin cascade, and renal and peripheral alterations attempt to restore both cardiac output and end-tissue perfusion. An adequate stroke volume cannot be ejected from the left ventricle, which shifts the whole pressure-volume relationship to the right (systolic failure). Adequate filling cannot be realized due to diastolic stiffness, which shifts the diastolic pressure-volume curve upward without affecting the systolic pressure-volume curve (diastolic failure). Left ventricular heart failure is the dominant picture of heart failure syndrome, but the right heart can develop isolated failure as well. Biventricular failure is mostly an end-stage clinical situation of the heart failure syndrome. More recently, the rise in the incidence of right ventricular failure can be seen after the implantation of a left ventricular assist device. This chapter clarifies and presents pathophysiologic alterations in heart failure syndrome.
heart failuresystolic dysfunctiondiastolic dysfunctionmyocardial stiffnessventricular dilatationneurohormonalrenin-angiotensinnorepinephrine
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Heart failure is an epidemic contributing considerably to the overall cost of health care in developed and also developing countries. Heart failure syndrome (HFS) is the currently accepted term describing a systemic disease affecting several organs, creating high morbidity and mortality rates due to the heart’s inability to supply oxygenated blood, including metabolites, to end organs and peripheral tissues (Table 1) . Pathophysiological Mechanisms leading to Heart Failure Essay. Acute event or acute refractory form of chronic heart failure can be fatal, whereas chronic prognosis is characterized by terminal congestive heart failure symptoms. The failing heart strives to balance “preload” and “afterload” for compensation of impaired contractility and to deter the development of congestion using a myriad of mechanisms.
(1) Activated feedback signals from peripheral reflex circuit
b. Anabolic blunting (proteolysis)
c. Insulin resistance (>50% reducing normal anabolic responses)
d. Oxygen radical accumulation
(2) Global metabolic imbalance (increased catabolic/anabolic imbalance)
(3) Systemic dysregulation of several hormonal pathways
(4) Multi-organ dysfunction (hyperbilirubinemia, uremia, anemia, hypoalbuminemia, etc.)
(5) Development of sarcopenia and cachexia
Heart failure syndrome as a multisystem disease.
1. Left heart failure
Left heart failure (LHF), with any structural and/or functional cardiac abnormalities, is a complex clinical state characterized by left ventricular pump dysfunction and related clinical symptoms (dyspnea, fatigue, exercise intolerance, etc.), including signs of volume overload (pulmonary crackles, peripheral edema, etc.) . All steps of energy extraction, transfer, and utilization are affected, with metabolic failure being the important underlying pathophysiologic mechanism causing first myocardial and then systemic decompensation . The pathophysiologic state perpetuates the progression of the failure, regardless of the precipitating event via several compensatory mechanisms. Compensatory mechanisms exist on every level of this scenario to restrain the clinical symptoms via correction of the global imbalance between the catabolic and anabolic status; however, they can lead to further myocardial deterioration and worsening HFS. Pathophysiological Mechanisms leading to Heart Failure Essay.
The most important classification of LHF is dependent on whether the left ventricular ejection fraction (LVEF) is reduced or preserved. The standard relationship between intracavitary volume and pressure values is affected in heart failure, and left ventricular pressure-volume curves change according to the failure type (Figure 1). In systolic LHF, an adequate stroke volume cannot be sustained due to reduced ventricular systolic contractile function, which shifts the whole pressure-volume relationships to the right. In diastolic LHF, an adequate filling cannot be realized due to diastolic stiffness (poor ventricular compliance, impaired relaxation, worsened end-diastolic pressure), which shifts the diastolic pressure-volume curve upward; however, the systolic pressure-volume curve does not change.
Left ventricular pressure-volume relationships: the green line represents the diastolic pressure-volume relationship, and the red line represents the end-systolic pressure-volume relationship. Both curves are shifted to the right in dilated CMP (blue arrow), to the left in hypertrophic CMP (green arrow), and only diastolic curve is shifted upward in restrictive CMP (red arrow). CMP, cardiomyopathy; LAP, left atrial pressure; LVEDP, left ventricular end-diastolic pressure; LVEDV, left ventricular end-diastolic volume; LVEF, left ventricular ejection fraction; LVESP, left ventricular end-systolic pressure; LVESV, left ventricular end-systolic volume; SAP, systolic aortic pressure; SV, stroke volume.
From asymptomatic to symptomatic stages, several counterregulatory mechanisms are activated (Table 2). First, inadequate stroke volume induces sympathetic nervous system activation, which increases cardiac contractile frequency and strength. Pathophysiological Mechanisms leading to Heart Failure Essay. This chronotropic effect leads to enhancement of total stroke volume per minute via increasing heart rate frequency, but this positive effect is reversed after tachycardia reaches a threshold of 140–150 beats/min (Figure 2). The next step is the augmentation of intravascular volume via neurohormonal system activation, which results in increasing intravascular volume, enlarging ventricular chambers, and improvement in myocardial fiber tension . The inotropic effect via the Frank-Starling mechanism increases myocardial contraction power, but this positive effect reverses after the sarcomere length reaches the upper limit of 2.2 μm (Figure 3). At this stage, no physiologic mechanism can improve the contractility, stroke volume, and cardiac decompensation, and the left ventricle (LV) undergoes progressive alterations from reversible cellular to irreversible myocardial remodeling. The heart is a self-renewing organ, characterized by an increase in myocyte turnover rate during pathological stress, especially in heart failure. The turnover mechanism becomes overwhelmed by a faster loss of myocytes, and this unfavorable imbalance causes the progression of ventricular remodeling during heart failure.
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Relationship between cardiac output and heart rate (chronotropy; Bowditch effect).
Relation between cardiac output and left ventricular filling (inotropy; Frank-Starling effect).
1.1. Morphological changes
Any of the cardiac pathology causing myocardial dysfunction results in abnormal myocyte growth, with a resultant cascade of gene activation stimulating cardiac remodeling. The hallmarks of cardiac remodeling are myocardial cell hypertrophy and cardiac dilatation with increased interstitial matrix formation. Pathophysiological Mechanisms leading to Heart Failure Essay. This compensatory mechanism to preserve contraction capability shifts to a maladaptive process after a cutoff level and contributes to the worsening of heart failure during myocardial degenerative progression. Progressive necrotic, apoptotic, or autophagic myocyte loss may contribute to worsening cardiac dysfunction and left ventricular remodeling. Changes within the extracellular matrix such as fibrillary collagen synthesis and degradation, loss of collagen struts, and collagen cross-linking characterize subsequent myocardial adaptation during cardiac remodeling. Cardiac fibroblasts are transformed into myofibroblasts and migrate into the area surrounding injured tissues to secrete collagen and restrict the injured site by scar formation (myocardial fibrosis). Pathophysiological Mechanisms leading to Heart Failure Essay.