The adaptive mechanisms may be short term ones which come into play within minutes or hours of the onset of myocardial dysfunction. These are:
Frank-Starling Mechanism
In the Frank-Starling mechanism increased preload helps in sustaining cardiac performance. Starling’s law essentially means that stroke volume is related to the end-diastolic volume. Frank proposed that the greater initial left ventricular volume leads to more rapid rate of rise of pressure, greater peak pressure and faster rate of relaxation. So the Frank-Starling law accounts for increased inotropic state and increased diastolic filling.
Neuro Hormones
Activation of neurohumoral systems resulting in release of noradrenaline leading to augmentation of myocardial contractility.
Renin-Angiotensin-Aldosterone System Activation of renin-angiotensin-aldosterone system which helps in maintaining arterial pressure and perfusion of vital organs.
Myocardial Hypertrophy and Remodeling
The long term adaptive mechanisms involve myocardial hypertrophy and remodeling which occurs slowly over weeks to months.The capacity of these adaptive mechanisms meant to sustain cardiac performance is not infinite and over a period of time maladaption sets in. Short term effects are mainly adaptive and occur in acute heart failure whereas long term effects are mainly deleterious and occur in chronic heart failure. For example, salt and water retention augments preload as short-term effect but causes pulmonary congestion and edema in the long term. Vasoconstriction helps to maintain blood pressure and perfusion of vital organs but it aggravates pump dysfunction by increasing afterload.Sympathetic stimulation increases heart rate and stroke volume but also increases energy expenditure. Hypertrophy helps to unload individual muscle fibers but leads to death of cardiac cells and cardiomyopathy of overload.
Sympathetic Activity
In heart failure there is adrenergic activation and parasympathetic withdrawal. This results in increase in myocardial contractility, tachycardia, sodium retention, renin release and generalized
vasoconstriction.
Renin-Angiotensin System (RAS)
As heart failure sets in, there is activation of RAS (Fig 2.1). Adrenergic stimulation of beta-1 receptors in juxtaglomerular apparatus of the kidneys results in release of renin. Another mechanism i.e. responsible for renin release is baroreceptor stimulation in renal vascular bed by reduction of renal blood flow.
Angiotensin II that is released is a powerful vasoconstrictor and stimulates the release of aldosterone. It also causes remodeling of cardiac myocytes. Aldosterone retains sodium and has direct effects on myocardium. The result is increased systemic vascular resistance and development of edema. Hence the interruption of this renin-angiotensin-aldosterone axis by angiotensin-converting enzyme inhibitors (ACE-Inhibitors) or angiotensin receptor blockers(ARBs) has salutary effects as there is reduction in systemic vascular resistance, afterload reduction, mild diuresis and improvement in the cardiac output.Angiotensin II also has direct role in modifying the structure and function of myocardium
Myocardial Hypertrophy and Remodeling
The long term adaptive mechanisms involve myocardial hypertrophy and remodeling which occurs slowly over weeks to months.The capacity of these adaptive mechanisms meant to sustain cardiac performance is not infinite and over a period of time maladaption sets in. Short term effects are mainly adaptive and occur in acute heart failure whereas long term effects are mainly deleterious and occur in chronic heart failure. For example, salt and water retention augments preload as short-term effect but causes pulmonary congestion and edema in the long term. Vasoconstriction helps to maintain blood pressure and perfusion of vital organs but it aggravates pump dysfunction by increasing afterload.Sympathetic stimulation increases heart rate and stroke volume but also increases energy expenditure. Hypertrophy helps to unload individual muscle fibers but leads to death of cardiac cells and cardiomyopathy of overload.
Sympathetic Activity
In heart failure there is adrenergic activation and parasympathetic withdrawal. This results in increase in myocardial contractility, tachycardia, sodium retention, renin release and generalized
vasoconstriction.
Renin-Angiotensin System (RAS)
As heart failure sets in, there is activation of RAS (Fig 2.1). Adrenergic stimulation of beta-1 receptors in juxtaglomerular apparatus of the kidneys results in release of renin. Another mechanism i.e. responsible for renin release is baroreceptor stimulation in renal vascular bed by reduction of renal blood flow.
Angiotensin II that is released is a powerful vasoconstrictor and stimulates the release of aldosterone. It also causes remodeling of cardiac myocytes. Aldosterone retains sodium and has direct effects on myocardium. The result is increased systemic vascular resistance and development of edema. Hence the interruption of this renin-angiotensin-aldosterone axis by angiotensin-converting enzyme inhibitors (ACE-Inhibitors) or angiotensin receptor blockers(ARBs) has salutary effects as there is reduction in systemic vascular resistance, afterload reduction, mild diuresis and improvement in the cardiac output.Angiotensin II also has direct role in modifying the structure and function of myocardium
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| Renin-angiotensin system |
Natriuretic Peptides
There are three natriuretic peptides—atrial (ANP) stored mainly in the atrium, brain (BNP) stored mainly in the ventricular myocardium and C-natriuretic peptide (CNP) located primarily in the vasculature.
Circulating levels ANP and BNP are elevated in heart failure. They are vasodilatory and natriuretic.
There are three natriuretic peptides—atrial (ANP) stored mainly in the atrium, brain (BNP) stored mainly in the ventricular myocardium and C-natriuretic peptide (CNP) located primarily in the vasculature.
Circulating levels ANP and BNP are elevated in heart failure. They are vasodilatory and natriuretic.
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