Pathophysiology of Congestive Heart Failure- CardioRush

Heart failure
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Depressed contractility, poor systolic ejection, poor muscle perfusion, myopathy, exercise intoleranceWhat characterizes systolic heart failure?TrueTrue or false: though diastolic heart failure may occur without concurrent systolic failure, systolic failure is ALWAYS accompanied by diastolic failurePulmonary edema (LCHF), elevated jugular pressure, hepatic enlargement, cavitary effusions, peripheral edema (RCHF)What are the physical signs associated with high Na and water retention in CHF?Insult leads to decreased cardiac performance, reducing effective circulating volume, which results in neurohumoral activation to cause vasoconstriction and increased plasma volume, which increases preload and afterload, increased afterload causes decreased cardiac performanceWhat is the cycle that continues to make heart failure worse once it begins?Frank Starling mechanism, neurohumoral activation, myocardial remodeling and hypertrophyWhat are the 3 major adaptive mechanisms the heart can use to adapt to change in heart failure?MinutesHow long does it take for the frank starling mechanism to take effect to help adapt to cardiac changes?Increases preload to maintain COWhat does the Frank Starling mechanism cause to adapt to cardiac change?Minutes to hoursHow long does it take for the Neurohumoral activation mechanism to take effect to help adapt to cardiac changes?Weeks to monthsHow long does it take for the myocardial remodeling and hypertrophy mechanism to take effect to help adapt to cardiac changes?For any given afterload, contractility and SV will be greater with an increased preloadWhat does Starling's law of the heart state?End diastolic wall stressWhat is preload?End systolic wall stressWhat is afterload?Ca sensitization via length dependent activation of sarcomere with stretchBy what mechanism does an increase in preload cause an increase in contractility and SV?Normal heart is preload dependent, can achieve normal cardiac function without congestion, failing heart cannotWhat is the shape of the starling curve in a normal heart vs. a failing heart in response to an increase in preload?False (failing heart is less preload dependent)True or false: the cardiac output of the failing heart is more preload dependent/responsive than the normal heartIncreased SVWhat is the result of an increased preload in a normal heart?TrueTrue or false: the failing heart is more afterload dependentCardiac output affected more by changes in afterload than preloadWhat does it mean by the failing heart being more afterload dependent?RAAS, ADH, SNS, baroreceptors, endothelins, inflammatory mediators, natriuretic peptidesWhat are the components of neurohumoral activation in CHF?Na and water retention, vasoconstrictionWhat is the end result of RAAS activation?Hyponatremia, SNS stimulation, decreased renal perfusionWhat triggers renin release from the kidney?Increase in BP and BVWhat is the net effect of RAAS activation?Remodeling, progressive hypertrophy, fibrosisWhat does the intra cardiac RAAS system cause when activated?Potent vasoconstriction, renal Na/water resorption, aldosterone and ADH release, SNS stimulation, myocardial hypertrophy and fibrosisWhat are the effects of antiogensin II?GPCR activation increases cAMP, increases Ca, increases TPR and afterloadWhat is the result of vasoconstriction as mediated by angiotensin II?Renal Na/water retentionWhat is the main effect of aldosterone?Myocardial hypertrophy and fibrosis, vascular remodeling, indirect vasoconstrictionWhat are some secondary effects of aldosterone?Diastolic dysfunctionWhat does aldosterone mediated myocardial hypertrophy and fibrosis lead to?Reduced vascular compliance, endothelial dysfunctionWhat is the result of aldosterone mediated vascular remodeling?Increased catecholamine sensitivity, increased pressor response to AT-IIWhat is the result of aldosterone mediated indirect vasoconstriction?Hyperosmolarity, AT-II, SNS stimulation, decreases volume, nauseaWhat triggers ADH (arginine vasopressin) release?V1, V2What are the 2 receptors for ADH?Potent vasoconstrictionWhat is the effect of V1 binding by ADH?Increased free water reabsorption by aquaporins in collecting ductsWhat is the effect of V2 binding by ADH?TrueTrue or false: ADH contributes to CHF signs by causing dilutional hyponatremia from too much water reabsorptionCongestion, increased afterload, dilutional hyponatremiaWhat are the signs that ADH causes in CHF?False (they are central to the pathophys of CHF)True or false: fluid and Na retention don't play a major role in CHFDecreased Na and water loss lead to increased preload and afterload, signs of congestionHow does the kidney contribute to signs of CHF?Cardio renal syndromeWhat describes the complex, multifactorial interplay between the heart and kidney in CHF?TrueTrue or false: The heart and kidneys contribute to a cycle that leads to the progressive worsening of CHFElastic arteries, large veins, heartWhere are baroreceptors located in the body?Inhibits SNS stimulationWhat does stretch of a baroreceptor usually cause?BluntingWhat is the effect of heart failure on the baroreceptors?Increased Na/K ATPase activityWhat is baroreceptor blunting in HF associated with?Myocardial failure reduces CO, leads to relative hypotension, baroreceptors fire, signal to vasomotor center to increase SNS activation and decrease vagal toneWhat is the pathway that leads to adrenergic activation in heart failure?Increased circulating catecholamines, vasoconstriction, increased inotropy, renal stimulation, maintains BP, CO, tissue perfusionWhat is the acute effect of SNS activation in response to low BP?Heart toxicityWhat is the longterm result of excessive SNS stimulation in heart failure?Beta receptor down regulation and uncompling, depletion of myocardial NorEpi, impaired contractile function, myocyte apoptosis causing remodeling and fibrosisHow does adrenergic excess lead to myocardial desensitization to catecholamines?Intracellular Ca overload, delayed diastolic Ca decrease, increase O2 demand, increased apoptosis and necrosis, renin release triggered, further damaging myocardiumWhat causes myocardial toxicity with excess catecholamines?Arrhythmogenesis, impaired relaxation causes diastolic dysfunctionWhat does the intracellular Ca overload and delayed diastolic Ca decrease lead to in heart failure?TrueTrue or false: if an animal presents with signs of SNS stimulation, you should investigate for HF, as SNS stimulation is a common signSNS, AT-II, AVP, endothelinsWhat signals lead to vascular remodeling and increased vascular resistance in CHF?Normal blood flowWhat is required for appropriate endothelial function?Less NO, more endothelin releasedWhat is the result of endothelial damage and dysfunction on NO and endothelin?IncreaseWhat happens to the levels of endothelin in CHF?Myocardium, endothelial cellsWhere is endothelin released from in CHF?AT-II, endothelial injuryWhat is the main stimuli for endothelin release?Potent vasoconstrictionWhat is the result of endothelin release?Increased afterloadWhat is the result of potent vasoconstriction from endothelin release?Ca overload, inotropic and mitogenic effectsWhat are the toxic effects of endothelin on the myocardium?NOWhat is released normally from endothelium in response to shear stress from blood flow?Guanylate cyclase activation, increased cGMP, vasodilationWhat is the result of NO release?Decreases due to endothelial dysfunctionWhat happens to the levels of NO release in heart failure?Increased vascular resistance, increased afterload, increased MVO2What is the result of decreased ability to release NO in heart failure?False (has been shown)True or false: Systemic inflammation has not been shown to be a major risk factor in people for developing CHFIncreaseWhat happens to the levels of proinflammatory cytokines with HF?TrueTrue or false: Proinflammatory cytokines are beneficial at physiologic levels, but maladaptive effects occur at supraphysiologic levelsTNF-alphaWhat is a major proinflammatory cytokine that increases with AT-II?Cardiac remodeling, decreased inotropy, systemic inflammation and cachexiaWhat are the effects of TNF alpha release in HF?Short term inotrope, acute cytoprotection, tissue repair following ischemic injuryWhat are the beneficial effects of proinflammatory cytokines at physiologic levels?Delayed negative inotropy, ventricular dilation, myocardial fibrosis, progression of CHFWhat are the detrimental effects of proinflammatory cytokines in heart failure?ANP, BNPWhat are the 2 main natriuretic peptides?Increased ventricular wall stressWhat is BNP released in response to?Diuresis, natriuresis, vasodilationWhat are the main effects of BNP?TrueTrue or false: natriuretic peptides directly counter the effects of RAAS activationFalse (RAAS and SNS often overpower NPs)True or false: Because natriuretic peptides counteract RAAS, they are often able to balance out the effects in heart failurePotent natriuresis, diuresis, balanced vasodilation, antagonize RAAS and SNS, inhibit aldosterone and ADH, reduce ventricular hypertrophy and fibrosis, diagnostic and therapeutic usesWhat are the actions of netriuretic peptides?(Pressure x radius)/2(thickness)What is the equation for wall stress?Concentric hypertrophyWhat is the response of the myocardium to pressure overload?Eccentric hypertrophyWhat is the response of the myocardium to volume overload?End systolicWhat increases with pressure overload: systolic or diastolic wall stress?Increased cell thicknessWhat changes occur in cells to result in concentric hypertrophy?End diastolicWhat increases with volume overload: systolic or diastolic wall stress?Cell lengthWhat changes occur in cells to result in eccentric hypertrophy?ParallelHow are sarcomeres added in concentric hypertrophy from pressure overload?In seriesHow are sarcomeres added in eccentric hypertrophy from volume overload?Injury, compensated, decompensatedWhat are the 3 stages of hypertrophy?Increased LV end diastolic volume, pressure back up, decreased forward SV, neurohormonal activation, volume overload hypertrophy to increase compliance to accomodate more volume, hyperdynamic state results in decreased filling pressureWhat is the pathway to respond to volume overload, such as in the case of mitral regugitation, to compensate?Continued Na and water retention, compliance limits reached in myocardium, decreased contractility and forward SV, increased filling pressure, pressure backs up into pulmonary capillaries and produces pulmonary edemaWhat happens in the decompensation state of volume overload hypertrophy?LA pressure increases, results in higher pulmonary circuit pressure, increased fluid transudation, acute or severe elevations in LA pressure cannot be compensated by the lymph drainageWhy does pulmonary edema develop with left heart failure and volume overload?Pleural effusion, pericardial effusion, ascitiesWhat are the signs associated with right sided CHF?TrueTrue or false: cats can develop pleural effusion in right OR left sided CHF