Pathophysiology of CHF I and II Flashcards
What is necessary to make the diagnosis of heart failure: low left ventricular ejection fraction, symptoms of exercise intolerance, presence of heart murmur
exercise intolerance
Pathophysiologic state in which the heart is unable to pump blood at a rate commensurate with the body’s requirements OR can only do so from an elevated filling pressure.
heart failure
What does the definition of heart failure have to do with left ventricular ejection fraction?
NOTHING –> you can classify HF on basis of LVEF but LVEF function doesn’t define HF
Is heart failure acute or chronic?
either
What heart failure stage? high risk patients (htn, diabetes, coronary disease, family history, cardiotoxic drugs)
A
What heart failure stage? prior or current symptoms
C
What heart failure stage? structural heart disease (LVH, MI, low LVEF, dilatation, valvular disease)
B
What heart failure stage? refractory
D
What is the difference between heart failure stage and class?
classes have to do with categorizing symptoms once you have them, stages have to do with estimating prognosis
What heart failure class? symptoms at rest
4
What heart failure class? symptoms with mild exertion
3
What heart failure class? symptoms with strenuous exertion
2
What heart failure class? asymptomatic
1
Gender and heart failure?
men get it early, women overtake by 75. women do better.
What is HFrEF?
heart failure with reduced ejection fraction (<=40%) AKA systolic HF
What is HFpEF?
heart failure with preserved LVEF (>=50%) AKA diastolic HF
What is HFpEF borderline and improved
HFpEF, borderline = heart failure with 41-49% LVEF
HFpEF, improved = heart failure with >40% LVEF but used to be lower
What is the consequence of increasing preload in HF?
normally preload is increased to improve CO –> in HF, the starling curve is an upside down U AKA at high left ventricular filling pressure (as preload increases) the heart decompensates (abnormally) so increasing preload doesn’t really help –> the whole curve is also shifted down so even at lower filling pressures, increasing preload has relatively less effect than in a normal heart
What are the symptoms of volume overload in HF
heart tries to increase pressure to improve CO (via preload) –> fluid backs up b/c of decompensated starling curve –> pulmonary congestion (cough, dyspnea), visceral congestion (bloating, swelling), peripheral edema, JFD, +HFR, ascites, anasarca, diffuse/displaced apex w/gallop rhythm
Process by which ventricular size, shape, and function are regulated by mechanical, neurohormonal, local, systemic, and genetic factors.
ventricular remodeling
3 ways heart can respond to hemodynamic burden
- use starling mechanism/preload to increase cross bridge formation (limited and leads to dilatation)
- augment muscle mass (remodeling and hypertrophy)
- recruit hormones to augment contractility (deleterious if used chronically)
What kind of hypertrophy? pressure overload
concentric
What kind of hypertrophy? volume overload
eccentric –> think about a balloon filling up causing the heart to get bigger w/o making wall thicker
What is LVEF in concentric hypertrophy?
usually normal –> pressures are higher but heart is stronger so don’t really affect ejection fraction –> but still have congestion, etc.
What happens to the interpapillary distance in a dilated heart?
increases –> also stretch annulus of valve –> leads to mitral valve regurgitation
What happens to conduction in those with a dilated heart?
have increased incidence of left bundle branch block leading to QRS elongation
What are the effects of LBBB on ventricular function?
- delayed mitral/aortic valve opening/closure
- prolongation of left ventricular isovolumic contraction time
- loss of interventricular syncrhony
- abnormal diastolic function
- paradoxical septal motion
etc. etc –> leads to further remodeling/progression of disease
What receptors are downregulated in situations involving cardiac dysfunction?
beta receptors –> abnormal myocyte function
What receptors are implicated in increased renal sympathetic activity in heart failure that contribute to sodium retention, activation of RAS, and ultimately, disease progression?
beta1, alpha1
What receptors are implicated in increased vascular constriction in heart failure and ultimately, disease progression?
alpha1
What receptors are implicated in increased cardiac sympathetic activity in heart failure that contribute to myocyte hypertrophy, myocyte injury, increased arrhythmias, and ultimately, disease progression?
beta1, beta2, alpha1
Angiotensin II is a positive/negative inotrope.
positive –> leads to LV growth, hypertrophy, remodeling in the long term
How does angiotensin ii potentiate fibroblast activity in the heart?
ag II –> IP3/PKC –> calcium + aldosterone –> corticoid receptor = genes for collagen/interstitial fibrosis
What are the two mechanisms by which secondary aldosteronism occurs in CHF?
- increased ZG production due to increased plasma angiotensin stimulation
- decreased hepatic clearance b/c of reduce hepatic perfusion
What is the prime directive of arginine vasopressin?
maintain volume to maintain CO (via increasing SVR and reducing free water clearance in kidney)
How does the heart counter regulate the sympathetic inflow?
- reduce beta receptors
- increase inhibitory g protein
- reduce atp stores to prevent cAMP from allowing inflow of calcium
- counter regulatory natriuretic peptides
What does ejection fraction have to do with BNP?
nothing –> BNP is related to wall stress (LVEDP)
What is the function of natriuretic peptides?
oppose vasoconstrictive and salt/water retention of activated RAS and sympathetic system
3 ways to pharmacologically limit effects of AG II
- ACE inhibitor
- AR blocker
- aldosterone antagonist
T/F the use of ACE-I and ARBs can reduce disease progression in CHF
T –> as measured by LV size and mass
T/F the use of aldosterone antagonists can reduce disease progression in CHF
T –> better survival
T/F the use of beta1 selective blockers can reduce disease progression in CHF
T –> better survival and fewer symptoms, better LVEF
T/F the use of combined beta/alpha blockers can reduce disease progression in CHF
T –> better LVEF and survival
Side effects of beta blockers
fatigue and low bp –> have to scale the dose up slowly
Indications for CRT
symptomatic heart failure, LVEF150msec (LBBB)
Short-term effects of CRT
increased LVEF, reduced LVEDD