Heart failure Flashcards
What does the tension that build up during isometric contraction equals to? How does stretching the cardial muscle help it contract?
During isometric contraction, the total tension (sum of active plus passive tension) generated by the fibers is proportional to the length of the muscle at the time of stimulation. Stretching the muscle before stimulation optimizes the overlap and interaction of myosin and actin filaments, increasing the number of cross bridges and the force of contraction. Stretching cardiac muscle fibers also increase the sensitivity of myofilament to calcium, which further augments force development.
what determines the final length of the muscle after contraction?
In this situation, the final length of the muscle at the end of contraction is determined by the magnitude of the load but is independent of the length of the muscle before stimulation. (1) The tension generated by the fiber is equal to the fixed load; (2) the greater the load opposing contraction, the less the muscle fiber can shorten; (3) if the fiber is stretched to a longer length before stimulation but the afterload is kept constant, the muscle will shorten a greater distance to attain the same final length at the end of contraction; and (4) the maximum tension that can be produced during isotonic contraction is the same as the force produced by an isometric contraction at that initial fiber length.
What are the three determinant of stroke volume?
Preload, afterload and myocardial contractility
CO = SV X HR
What happens if the preload and contractility of the heart are held constant while the afterload is manipulated?
If the preload and contractility are held constant and afterload is manipulated, the pressure generated by the left ventricle during ejection increases. In this situation, more ventricular work is expended in overcoming the resistance to ejection and therefore less fiber shortening takes place. An increase in afterload results in a higher ventricular systolic pressure and a greater than normal LV ESV (stoke volume is reduced).. The greater the afterload, the higher the ESV
Why does the ventricle has a diminished capacity to eject blood during systolic dysfunction?
Because of impaired myocardial contractility (due to destruction of myocytes, abnormal myocyte function, or fibrosis) or pressure overload (excessive afterload).
Impaired contractility causes the ESPVR to shift downward such that systolic emptying ceases at a higher-than-normal ESV. When more blood is added to the ESV (from the pulmonary venous return), this increase both the volume and the pressure. While this increase in preload induces a compensatory rise in stroke volume, impaired contractility and the reduced EF cause the ESV to remain elevated. During diastole, the elevated LV pressure is transmitted to the left atrium and to the pulmonary veins and capillaries. An elevated pulmonary capillary hydrostatic pressure (<20 mm Hg), result in the transudation of fluid into the pulmonary interstitium.
How can acute myocardial ischemia lead to heart failure?
Acute myocardial ischemia is a condition that inhibits energy delivery and diastolic relaxation.
How can acute left ventricular hypertrophy, fibrosis lead to heart failure?
Left ventricular hypertrophy, fibrosis or restrictive cardiomyopathy cause the LV walls to become chronically stiffened.
When does the right ventricle fails?
When there is an increase in afterload
What the effect of right ventricle failure on the left ventricle?
The decreased right ventricular output reduces blood return to the left ventricle, causing the ventricular stroke volume to decline.
What are the condition that causes right-sided heart failure?
Cardiac causes –> Left-sided heart failure, pulmonic valve stenosis, Right ventricular infarction
Pulmonary parenchymal disease –> Chronic obstructive pulmonary disease, interstitial lung disease, Chronic lung infection.
Pulmonary vascular disease —> Pulmonary embolism and pulmonary arteriolar hypertension
What are the compensatory mechanism during heart failure?
Frank-starling mechanism
Heart failure causes a downward shift of the ventricular performance curve. At any given preload, the stroke volume is decreased, which result in incomplete chamber emptying. The increase in volume of blood that accumulates in the ventricle during diastole increase stretch of the myofibers, which induce a greater stroke volume on contraction, which helps empty the enlarged left ventricle and preserve forward cardiac output.
Neurohormonal alterations
Mechanisms activated in heart failure in response to decreased cardiac output: (1) the adrenergic nervous system (2) the renin-angiotensin-aldosterone system, and (3) increased production of ADH. These mechanisms increase systemic vascular resistance which helps to maintain arterial perfusion to vital organs.
Blood pressure = cardiac output X Total peripheral resistance
How does adrenergic nervous system regulate decrease in blood pressure?
Baroreceptor in the carotid sinus and aortic arch decrease their rate of firing in proportion to the fall in blood pressure, and the signal is transmitted by the 9th and 10th cranial nerve to the cardiovascular control center in the medulla. The sympathetic outflow to the heart and peripheral circulation is enhanced and the parasympathetic tone is diminished. (1) an increase in heart rate, (2) augmentation of ventricular contractility, and (3) vasocontraction of the systemic veins (Frank-starling) and arteries [increase vascular resistance to increase BP (BP = CO X SV)].
Explain the renin-angiotensin-aldesterone system? Where is renin secret? What is the stimuli for its secretion?
Renin-angiotensin-aldosterone system
Stimuli for renin secretion from the juxtaglomerular cells of the kidney in heart failure include (1) decreased renal artery perfusion pressure (2) decrease salt delivery to macula densa (3) direct stimulation of juxtaglomerular β-receptors by the activated adrenergic nervous system.
Angiotensin II constrict arterioles and raises total peripheral resistance, to increase blood pressure. Angiotensin II increase intravascular volume by: (1) at the hypothalamus, it stimulates thirst and water intake, (2) at the adrenal cortex, it acts to increase aldosterone secretion.
What is the function of ADH and how can it increase the blood pressure? Why is continuous stimulation bad during heart failure?
ADH secretion is mediated through arterial baroreceptor, and by increased levels of Angiotensin II. ADH also appears to contribute to systemic vasoconstriction. ADH continued activation is harmful, the increased circulating volume and augmented venous return to the heart may eventually worsen engorgement of the lung vasculature, exacerbating congestive pulmonary symptoms. Furthermore, the elevated arteriolar resistance increases the afterload against which the failing left ventricle contracts and may ultimately impair stroke volume and reduce cardiac output. In addition, the increased heart rate augments metabolic demand and can therefore further reduce the performance of the failing heart. Continuous sympathetic activation results in down-regulation of cardiac β-adrenergic receptors and up-regulation of inhibitory G proteins, contributing to a decrease in the myocardium’s sensitivity to circulating catecholamines and a reduced inotropic response.
What does elevated levels of angiotensin II and aldosterone do?
Elevated levels of angiotensin II and aldosterone provoke the production of cytokine, activated macrophages, and stimulated fibroblast, resulting in fibrous and adverse remodeling of the failing heart.
