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Topic: Afterload

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	Altered cardiac function
		This relationship between left ventricular systolic function and afterload forms the basis for afterload reduction therapy used in the treatment of systolic failure and congestive cardiac failure.
		Afterload is dependent on a variety of physiological factors relating to the body's vasculature and how it inter-relates with the left ventricle.
		Afterload is also increased by inappropriate peripheral vasoconstriction perhaps due to imbalances in the neuronal and local endothelium-dependent vasoconstrictor and vasodilator forces.
	www.rcsed.ac.uk /journal/vol46_1/4610005.htm (4133 words)

	Afterload - Wikipedia, the free encyclopedia
		Afterload can also be described as the pressure that the chamber of the heart has to generate in order to eject blood out of the chamber.
		In the case of the left ventricle, the afterload is a consequence of the blood pressure, since the pressure in the ventricle must be greater than the blood pressure in order to open the aortic valve.
		Aortic stenosis increases the afterload because the left ventricle has to overcome the pressure gradient caused by the stenotic aortic valve in addition to the blood pressure in order to eject blood into the aorta.
	en.wikipedia.org /wiki/Afterload (321 words)

	Shock (Site not responding. Last check: 2007-10-17)
		In hypovolemic shock, preload is decreased, afterload is increased, and the myocardial contractility remains normal.
		In early septic shock, the preload and afterload are decreased, and the myocardial contractility is increased.
		In late septic shock, the preload and afterload are increased and the myocardial contractility is decreased.
	home.coqui.net /myrna/shock.htm (2490 words)

	MedEdCenter (Site not responding. Last check: 2007-10-17)
		Afterload is the resistance against which the ventricles must pump blood.
		Afterload is determined by two conditions; the blood volume ejected from the ventricle and the compliance of the vascular space into which the blood is ejected.
		Contractility is an inherent capability of the myocardium to increase the extent and force of muscle fiber shortening independent of preload and afterload.
	www.mededcenter.com /module_viewer.asp?module=100 (3089 words)

	[No title] (Site not responding. Last check: 2007-10-17)
		Afterload - Increased tension on a muscle fiber after contraction begins; usually due to increased aortic/arterial blood pressure and/or decreased compliance; imposed during systole.
		Afterload, that load applied after a muscle begins to contract, alters stroke volume (Figure 2.03).
		At a great enough afterload the aortic valve fails to open and ejection is prevented, bringing external cardiac work to zero.
	www.coheadquarters.com /PennLibr/MyPhysiology/lect2/pen2.08.htm (108 words)

	eMedicine - Heart Failure : Article by Michael E Zevitz, MD
		The increase in afterload and myocardial contractility (known as inotropy) and the impairment in myocardial lusitropy lead to an increase in myocardial energy expenditure and a further decrease in cardiac output.
		Afterload reduction results in increased cardiac output and improved renal perfusion, which allows for diuresis in the patient with fluid overload.
		Afterload reduction is associated with increased cardiac output.
	www.emedicine.com /med/topic3552.htm (11115 words)

	Medical Pharmacology Topics
		Afterload is the pressure that has to be overcome by the contraction of the ventricle before the valve opens to expel the blood into the systemic circulation.
		Drugs that reduce both preload and afterload include nitroprusside, prazosin, ACE inhibitors and angiotensin II receptor blockers (the later two discused in the "Antihypertensives" section).
		Hydralazine is used to reduce afterload in patients with congestive heart failure and as an antihypertensive.
	www.angelfire.com /sc3/toxchick/medpharm/medpharm34.html (1082 words)

	Critical Care \| Full text \| Increasing afterload induces myocardial diastolic dysfunction
		This is an interesting paper that suggests that changes in afterload produce significant changes in diastolic performance and the authors comment that this may be further exacerbated in diseased heart.
		To investigate the hypothesis that an afterload elevation which increases relative load and markedly slows the rate of LVP fall would result in incomplete myocardial relaxation and in the upward shift of the end-diastolic pressure-volume relation, ie diastolic dysfunction.
		Elevated afterloads prolonged the half-life of LVP fall and caused an upward shift of the diastolic LVP-ID relation.
	ccforum.com /paperreport/ccf-1999-2081 (717 words)

	Acta Cardiologica - Abstract, vol.58 - nr. 4/6 - 2003 (Site not responding. Last check: 2007-10-17)
		RV and LV afterload elevations were performed by beat-to-beat graded constrictions of the pulmonary trunk or aortic root, respectively.
		In both ventricles, afterload modulation of dP/dt was assessed by dP/dtmax normalized for end-diastolic dimensions (dP/dtmax/EDD) and by peak and mean accelerations of pressure rise.
		RV afterload elevation increased dP/dtmax, dP/dtmax/EDD, peak and mean acceleration of RV pressure rise, without changing the time from end-diastole to dP/dtmax.
	www.actacardiologica.be /abstracts/abs5804200306.htm (280 words)

	VM8754: PATHOPHYSIOLOGY AND MEDICAL MANAGEMENT OF CONGESTIVE HEART FAILURE
		Afterload is the sum of all the external factors that oppose ventricular ejection.
		As afterload increases, more contractile energy must be devoted to generate tension to overcome the afterload rather than myocardial fiber shortening and ejection of adequate volumes of blood.
		When contractility is normal, elevating afterload leads to an increase in stroke work, with little elevation of ventricular end-diastolic volume or pressure and with little decline in stroke volume.
	education.vetmed.vt.edu /Curriculum/VM8754/xi.html (5875 words)

	The Effects of Barium, Dofetilide and 4-Aminopyridine (4-AP) on Ventricular Repolarization in Normal and Hypertrophied ...
		The cardiac output was increased to 60 ml/min
		The ordinate represents time, and differences in ventricular afterload are represented on the abscissa.
		afterloads in eight sham and eight hypertrophied hearts.
	jpet.aspetjournals.org /cgi/content/full/285/1/262 (5194 words)

	Congestive Heart Failure
		When the heart begins to fail and the CO is no longer sufficient to meet the metabolic demands of the body, three major compensatory mechanisms are activated: the adrenergic system, the renin-angiotensin-aldosterone system, and ventricular hypertrophy.
		This process is done in two ways: eccentric hypertrophy is due to volume overload causing the sarcomeres to replicate in a series causing fiber elongation and chamber enlargement; and concentric hypertrophy where increases in systolic wall stress causes sarcomere replication in parallel arrangement leading to ventricular wall thickness.
		Thiazides inhibit sodium-chloride transport, preventing the reabsorption of sodium in the cortical diluting segment at the ending portion of the loop of Henle and the proximal portion of the distal convoluted tubule.
	www.csufresno.edu /nursing/n140/studassign/chf.htm (4582 words)

	vasodilators
		This benefits patients in heart failure by reducing the afterload on the left ventricle, which enhances stroke volume and cardiac output and leads to secondary decreases in ventricular preload and venous pressures.
		Adding to this afterload effect is the influence of enhanced sympathetic stimulation due to a baroreceptor reflex in response to the fall in arterial pressure, which increases heart rate and inotropy.
		The effect of reducing afterload on enhancing cardiac output is even greater in failing hearts because stroke volume more sensitive to the influence of elevated afterload in hearts with impaired contractility.
	cvpharmacology.com /vasodilator/vasodilators.htm (1440 words)

	Heart Physiology : the WorldWide Intensivist
		A further load is then added (the "afterload") and the muscle is allowed to shorten when stimulated.
		As afterload increases, so ejection of blood slows and the volume ejected diminishes (for that beat).
		Despite the increased afterload, and the consequent increase in end-diastolic pressure (with normal stroke volume by the Starling effect), there is over subsequent beats a gradual fall in left-ventricular end-diastolic pressure, and stroke volume is nevertheless maintained!
	www.anaesthetist.com /icu/organs/heart/phys.htm (1232 words)

	Load as an acute determinant of end-diastolic pressure-volume relation -- Leite-Moreira and Correia-Pinto 280 (1): 51 ...
		Afterload elevations exceeding the relative load of the transition (80, 90, and 100% interventions) progressively slowed the
		Afterload elevations reaching or exceeding a relative load of 80% progressively shifted upward the ED P-ID relation.
		Afterload mismatch and preload reserve: a conceptual framework for the analysis of ventricular function.
	ajpheart.physiology.org /cgi/content/full/280/1/H51 (4283 words)

	Association of Veterans Affairs Anesthesiologists
		In the management of valvular heart disease, control of preload not only refers to control of end-diastolic volume, but also refers to the effects of left atrial pressure on the lungs and the effects of right atrial pressure on the body.
		In the management of valvular heart disease, control of afterload entails not only the control of MAP but also control of SVR.
		Decreased SVR tends to limit regurgitation by lowering diastolic pressure but the degree of afterload reduction may be limited by the decline in diastolic pressure.
	www.vaanes.org /FORUMS/ValvesAVAA.html (7571 words)

	AccessMedicine - Harrison's Internal Medicine: Ventricular Afterload
		In the intact heart the afterload may be defined as the tension or stress developed in the ventricular wall during ejection.
		Therefore, at any given level of aortic pressure, the afterload on a dilated left ventricle of normal thickness is higher than that on a normal-sized ventricle.
		Conversely, at the same aortic pressure and ventricular diastolic volume, the afterload of a hypertrophied ventricle is lower than of a normal chamber.
	www.accessmedicine.com /content.aspx?aID=80582 (300 words)

	Determinants of cardiac output:
		The stroke volume of the left ventricle is ultimately determined by the interaction between its preload, the contractile state of the myocardium and the afterload that the ventricle faces.
		In physiological terms, afterload can be defined as 'The sum of all those forces which oppose ventricular muscle shortening during systole' - although in a clinical sense it is probably more useful to consider systemic vascular resistance as the appropriate measure.
		As a result, 'afterload reduction' (reduction of systemic vascular resistance by the use of appropriate vasoactive drugs) is of the greatest benefit in those in whom myocardial function is most depressed.
	www.manbit.com /PAC/chapters/P42.cfm (879 words)

	Heart Failure - WSAVA 2002
		Increases in preload, afterload, sympathetic activation, and growth hormone activityinduce myocardial growth, whereas activation of RAS, prostaglandin E2, TGF-beta1, and insulin growth factor-1 induce remodeling of cardiac interstitium.
		Wall stress (a function of afterload), contractility, and heart rate are the main determinants of MVO2.
		Increase in afterload further decreases left ventricular function leading the organism into a new, decreased steady-state level, where the cardiac output is lower and vasoconstriction higher than would be optimal for the patient.
	www.vin.com /proceedings/Proceedings.plx?CID=WSAVA2002&PID=2524&Category=408 (1253 words)

	PHYSIOLOGY, BLOCK 2: JANUARY 1995 (Site not responding. Last check: 2007-10-17)
		As the afterload is increased, the velocity of shortening and the amount of shortening decrease.
		The velocity of shortening against a given afterload is related to the preload, which determines the resting length of the muscle.
		The afterload, which is the tension the myocardium must develop, is determined by the arterial pressure and the end-diastolic volume of the ventricle.
	condor.bcm.tmc.edu /MIEC/Syllabi/PhysB2/cardiac02.html (2862 words)

	[No title]
		The greater the afterload, the lower the rate of contraction (increased afterload (decreased shortening velocity) The greater the afterload, the lower the extent of contraction.
		fixed afterload, contractility increase contractility (use norepinephrine, digoxin, digitalis) fixed preload, afterload reduce afterload (discussed above) Q: “Uh.what are the units of preload and afterload?” A: The length/tension curve is related to the pressure/volume curve, and clinically, changes in wedge pressure are used to represent changes in the length of the muscle fibers, i.e.
		Afterload is tension or force and seems like it ought to be measured in newtons.
	www.uhmc.sunysb.edu /som/students/2003/Lectures/Cardio/cardio02.doc (2275 words)

	CV 32
		Increase in afterload (which tends to reduce stroke volume) tends to blunt the effects of the glycoside on contractility.
		In the patient having heart failure the improvement in cardiac function accompanies a decrease in peripheral resistance (afterload) which is due to a decrease in sympathetic activity.
		The long-term benefit of inotropic therapy is being debated and the present trend is to reduce afterload and inhibit the renin-angiotensin system (and sometimes beta blockade) rather than rely only on an inotrope in the management of chronic heart failure.
	www.umanitoba.ca /faculties/medicine/cardiology/cvnotes/cv32.htm (5790 words)

	Course:SOM/Block 4/Spring 2007/IQ 16/Week 1 Case 1 - CaseWiki
		In a pressure volume loop preload is estimated as end-diastolic volume (lower right corner; point 1)and afterload is estimated as end-sytolic volume (upper left corner; point 3); the end-diastolic pressure and end-systolic pressure are the pressures at which the EDV and ESV respectively occur.
		Afterload is increased in conditions like hypertension or stenosis; these conditions lead to an increase in LV pressure because more work is needed to overcome the resistance to ejection.
		The slope of the ESPVR is a function of cardiac contractility: as the contractility increases, the slope of ESPVR steepens.
	wiki.case.edu /Course:SOM/Block_4/Spring_2007/IQ_16/Week_1_Case_1 (3418 words)

	Nurse Bob's Hemodynamic Overview
		The resistance to the ventricular ejection, which is measured, by the pulmonary vascular resistance by the systemic vascular resistance, is afterload.
		Afterload can be managed by the manipulation of peripheral vascular resistance or systemic vascular resistance.
		That is, the lower the cardiac output the greater the afterload.
	rnbob.tripod.com /hemod.htm (4137 words)

	1.4.3 Control of cardiac output
		Afterload is the force against which the ventricles must act in order to eject blood.
		Factors which affect afterload are summarised in Table 1.1.
		The strength of the force of myocardial contraction is dependent on direct autonomic control affecting preload and afterload but also on the contractility of the myocardium.
	www.provet.co.uk /equinecardiology/5a583af.htm (1087 words)

	[No title]
		Since the afterload is kept constant, the maximum amount of tension reached is the same in both cases.
		Summary: Increased Preload with constant Afterload= Increased ventricular tension Increased ventricular pressure (initially) Resulting in Increased Aortic Flow (Ejection Fraction = stroke volume/Left Ventricular End Diastolic Volume(LVEDV)) Increase Afterload/ preload is constant IC The starting tension is constant for both control and variable since preload is constant.
		Increased Inotropic (contractile strength) state/ preload and afterload constant IC The final tension produced is unchanged since afterload and preload are constant.
	www.uhmc.sunysb.edu /som/students/2001/noteservice/h7.doc (2073 words)

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