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Flashcards in Heart Failure Pathophysiology 2 Deck (24):

Summarize the systems that are activated in response to heart failure that can be harmful in long term survival.

activation of neurohormones (increases vasoconstriction)
activation of renin-angiotensin system (increase in fluid retention)


Discuss the direct cardiovascular effects of RAS and the renal effects.

direct cardiovascular: increased contractility, hypertrophy, fibrosis (cardiac remodeling) and vasoconstriction

renal effects: predominant vasoconstriction at efferent arterioles, increased Na+ reabsorption, increased SNS activation and aldosterone, increased mesangial contraction


What are the long-term detrimental effects of the RAS activation? Discuss appropriate treatments.

initially to redirect blood flow, can cause cardiac fibrosis and after load can cause ventricular remodeling, mismatch of muscle and capillary density, water and salt retention

salt and water retention

appropriate control by ACE inhibitors, reduces mortality, hospitalizations and retards LV modeling (catopril, enalapril, lisinopril etc.)


Discuss the ill-effects of the SNS activation during heart failure.

NE increases HR, contractile force, speed of relaxation, and ventricular arrthymias, Ca++ overload in myocytes and myocyte death

SNS activates RAS system and acts a s net arterial vasoconstrictor


Discuss the detrimental long term effects of SNS activation. What are possible treatments?

initially increases CO output via HR and contractility and distributes blood to vital organs

has long-term detrimental effects by increasing ventricular arrhythmias, ventricular remodeling due to increased after load as well as myocyte damage, death and salt and water retention

treatment includes BBlockers because they can reverse remodeling (carvedilol, metroprolol succinate and bioprolol), and decrease mortality although then should not be used as a rescue therapy because they are negative ionotropes


What are the effects of aldosterone escape? How is it treated?

acute plasma increase, increasing heart and vascular stiffness, also potassium and magnesium loss can cause ventricular arrthymias, even with ACE-I

aldosterone blockade (spirolactone, eplereone) reduce death in patients with moderate to sever heart failure and this eiwth post MI systolic dysfunction, with danger of hyperkalemia


What are natriuetic peptides and why are they important to heart failure?

atrial natriuetic peptide (atrial)
brain natriuetic peptide (ventricular) are secreted in response to increased chamber pressure and wall stress, BNP is measured routinely because they act as mild vasodilators and mild diuretics by decreasing Na+ reabsorption in the proximal tubule (natriuresis)

intravenous human recombinant BNP can be given to increase vasodilation and relieve symptoms during decompensation


How are BNP levels use for diagnostic testing?

BNP levels can help to distinguish dyspnea as caused by heart failure and they serve as a marker of effective therapy as well possible prognostic tool; they are an imperfect test due false positives (older, renal disease, lung processes like PE or other lung disease)


What are the benefits and detriment of NO on the heart?

NO role in heart failure is unclear, suggest that NO has negative inotropic effects and mediate oxidative damage but may have beneficial cardiac effects due to localization; deficiency in vascular system in heart failure (particularly important for african american patients)


What are the deleterious effects of inflammatory mediators in HF?

increase LV dysfunction, pulmonary edema, cardiomyopathy, endothelial dysfunction, anorexia/cachexia


Contrast concentric and eccentric left ventricular hypertrophy.

in response to volume overload, chamber eccentrically expands via addition of sarcomere and myofibrils in series and chamber enlargement

in response to pressure overload, concentric hypertrophy leads to parallel addition of sacromeres and wall thickening


Due to vasoconstriction and volume retention there abnormal loading and myocardial dysfunction causing fibrosis and dilation and the process that predominates is ?

eccentric hypertrophy predominates, resulting in molecular changes occuring in all regions of the heart, even those distant form the infarction in ischemic cardiomypathy


What stimuli cause a switch to fetal gene program.

a to b myosin and altered cytoskeleton proteins occurs secondary to mechanical stress, neurohormones, inflammatory cytokines and ROS


How is the composition of channels altered in heart failure remodeling?

decreased SERCA bringing Ca back into ER
ryanodine receptor leaks Ca into the myoplasm

leading to slower kinetics due to decreased systolic Ca levels and increased diastolic Ca levels

during remodeling there is flat out myocyte necrosis and apoptosis


What treatments are known to address the molecular remodeling that occurs with heart failure?

ACE I, B blockers, aldosterone antagonist all can reverse the remodeling process at the anatomic and molecular levels, B blocker responsive patient might also increase levels of a myosin heavy chain


How does ventricular dilation effect the heart valves?

decreased response to filling in chronic decompensated heart is often complicated by valvular insufficiencies due to enlargement of chamber and annulus


Increased after load/ systemic pressure has what effect on the EF?

some of the stroke volume is pushed backwards through the pulmonary arteries and into the lungs increasing pulmonary wedge pressure, which reduces overall cardiac output


What is the goal dealing with fluid overload?

patient may be thirsty, but adding water to system may make things worse; solution lies in moving venous blood into the arteries via vasodilation, not failing heart is more sensitive to after load and has limited capacity to cope with increasing pressure


What are the key medical treatments in heart failure?

ACE I, and ARBs, Bblockers and aldosterone blockers; all which prevent worsening of left ventricle, prevent arrhythmia and sudden cardiac death, make people feel better and keep people alive longer


Discuss three device therapies and their primary action

1. implantable cardiac defibrillator to monitor and treat ventricular arrhythmias; can both pace and shock
2. biventricular pace maker to restore electrical and mechanical synchrony to dyssynchronous heart
3. left ventricular assist device (LVAD) to augment the ventricular function


Why is biventricular pacing particular helpful in bundle left branch block

because the septum contracts with the His purkinje system is it dyssynchronus with the free wall of the left ventricle and is a much less efficient pump

can improve stroke volume, mitral regurgitation and exercise tolerance (causing reverse remodeling)


What are the risks of an LVAD device

although it can increase perfusion to organs, there is risk with the operation to implant as well as danger of clotting, bleeding, stroke, LVAD dysfunction and non-pulsitile waveform can cause arterial pressure problems

only used as a end of life treatment or bridge to transplant


What are the benefits of a multi-disciplinary team approach to managing heart failure?

follow up can be improved, knowledge about patient tendencies is more keen and although it may not effect mortality, it may reduce hospital admissions and increase resource accessibility for patients


Systolic heart failure results in _____ physiologic responses to altered load ____ remodeling and _____ activation, all processes which contribute to disease progression and symptoms.

blunted physiologic response to altered load
adverse removing
neurohormonal activation