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Is low LVEF used to diagnose heart failure?

No, but it is used to classify it.


Is exercise intolerance important in the diagnosis of heart failure?



Definition of heart failure (HF)?

Heart is unable to pump enough blood to meet body's requirements OR can only do so at elevating filling pressures.


5 broad causes of heart failure?

Primary (something wrong with heart itself: ischemia, inflammation, valves, etc.).
Toxins (EtOH, adriamycin)


4 classic symptoms of HF?

Dyspnea, fatigue, exercise intolerance, and swelling.


What are stages A-D of HF?

A: high-risk patients
B: structural heart disease, but asymptomatic
C: symptomatic disease
D: treatment refractory disease


What are NYHA classes I-IV of HF?

I: asymptomatic
II: symptoms with moderate-strenuous exertion
III: symptoms with mild exertion
IV: symptoms at rest


Gender-age relationship of CHF?

Significantly more prevalent in men until about age 75... then it's more prevalent in women.


How does LV compliance vary between men and women?

Women tend to have less compliant hearts. (for a given volume, higher pressure)


How is heart failure with reduced LVEF (HFrEF) defined? What else is this called?

LVEF < 40%.
This is also called "systolic HF," because the problem is with getting blood out of the heart.


How is heart failure with preserved LVEF (HFpEF) defined? What else is this called?

LVEF > 50% (thus 40-50% is borderline)
This is also called "diastolic HF," because the main problem is with filling.


4 ways that the heart tries to increase CO in HF?

Increased preload.
Increased number of contractile elements (i.e. hypertrophy).
Increased HR.
Increased inotropy.


3 causes of symptoms of volume overload? (i.e 3 places to have congestion)

Pulmonary congestion (cough, dyspnea, orthopnea, PND).
Visceral congestion (abdominal bloating, swelling, early satiety, anorexia).
Peripheral edema.


Review: Contrast concentric vs. eccentric hypertrophy.

Concentric: relative wall thickness (RWT) increases, lumen narrows. Seen in hypertension (i.e. too much afterload).
Eccentric: RWT decreases, lumen increases. Seen in volume overload.


Why does dilated cardiomyopathy mess up heart valves?

This changes the angle in which the papillary muscles pull on the valve leavelets, causing them to pull open -> mitral regurgitation.


5 mechanical processes disrupted in Left Bundle Branch Block (LBBB)?

Delayed mitral and aortic opening/closure.
Prolonged LV isovolumetric contraction.
Loss of intraventricular synchrony.
Los of interventricular synchrony.
Abnormal diastolic function.


5 hemodynamic sequelae of the mechanical disruptions caused by LBBB?

Reduced LVEF.
Paradoxical septal motion (septum moves toward RV).
Reduced CO and MAP.
Increased LV filling rate and volume.
Increased duration of mitral regurgitation.


3 principal hemodynamic changes in HF?
What is the "neurohormonal stimulation" of HF trying to accomplish?

Increased ventricular wall stress.
Atrial hypertension due to diastolic dysfunction and fluid overload.
Reduced CO.

Neurohormonal stimulation is trying to restore CO.


Neurohormal stimulation to increase CO... is this a better short-term or long term thing?

It's better for short-term fight or flight, hemorrhage, etc. because it increases inotropy and HR.
In the long term, it causes LV remodeling and arrhythmias.


How does circulating plasma NE in HF correlate with survival?

Higher NE, less survival.


Agonism of which adrenergic receptor(s) cause myocyte hypertrophy, myocyte injury, and increased arrhythmias?

Beta-1, beta-2, and alpha-1.


Agonism of which adrenergic receptor(s) is mainly responsible for vasoconstriction?



Agonism of which adrenergic receptor(s) causes activation of RAS?

Beta-1 (apparently alpha-1 directly stimulates Na+ retention)


What effects does A-II have on heart, adrenals, and brain?

Heart: positive inotrope/chronotrope. LV growth/hypertrophy/remodeling.
Adrenal: Increased aldosterone release -> Na+ and H2O retention.
Brain: Potentiates sympathetic activation. Stims ADH release. Stimulates thirst and Na+ appetite. (etc.)


Review: What does ACE do aside from converting A-I to A-II?

It breaks down bradykinin.


What effects does A-II have on kidneys?
On vasculature?

Constricts afferent and efferent vasculature..... stimulates Na+ and bicarb resorption...(renal stuff)

A-II causes hypertrophy of vascular smooth muscle.


Does A-II play a role in causing interstitial fibrosis of the heart?

Yes, and so does aldosterone. They act on fibroblasts and turn on genes for collagen.


2 mechanisms for secondary aldosteronism (high aldo) in CHF?

CHF -> high A-II. A-II stimulates production by zona glomerulas.
Decreased hepatic clearance of aldo due to decreased hepatic blood flow.
(this makes patients very thirsty and crave salt)


Role of ADH aka. arginine vasopressin in HF?

Compensation to try to increase CO by increasing volume.
It increases SVR (which... would actually decrease CO...)
and reduces free water clearance by kidney.


Does antagonizing vasoconstrictive cytokines like endothelin, TNF-alpha, and IL-6 seem to help HF?

No. (it might help people feel better though)


Several ways that endothelial dysfunction may contribute to HF?

Less NO (EDRF) synthesis, increased NO clearance.
Increased ACE activity.
Increased sensitivity to endothelin.
Defective muscarinic receptors?


How does skeletal muscle tend to change?

Reduced oxygen utilization by mitochondria (even if there's no actual hypoxia).
Decreased strength due to decreased muscle bundle cross-sectional area.


How does the heart protect itself against chronic adregneric stimulation? (3 ways)

Beta receptors are downregulated after chronic stimulation.
Gi activity is increased (counteracts beta-induced Gs).
ATP depletion -> less cAMP for PKA activation -> less Ca++ in cardiac myocytes.


Review: What counterregulatory signaling molecules does the heart itself produce?

The atria (and ventricles?) produce ANP and BNP, which oppose RAAS.
(recall that BNP is a useful marker of wall stress)


Where, specifically, in the heart are ANP and BNP produced? What is the stimulus?

ANP: by atria in response to atrial distension (high preload)
BNP: by ventricles in response to overload (high LVEDP/ afterload)


In eccentric hypertrophy, do myocytes increase in length or in thickness?

In length


If the goal of natural compensatory mechanisms is to increase CO at any cost, what is goal of treatment of HF?

Prevent or reverse disease progression (which may involve opposing those compensatory mechanisms).
and of course... improve survival and symptoms.


How can you target the RAAS with meds? (3 ways)

ACE inhibitors (first line) - e.g. enalapril
Angiotensin receptor blockers "ARBs" (if can't tolerate ACE inhibitors)
Aldosterone antagonists (reserved for very symptomatic pts) -e.g. spironolactone


What are the effects of a beta-1 specific beta-blocker?
Example of such a drug?

Blocks the inotropic, hypertropic, arrythmogenic effects on heart.
Inhibits RAAS activation.
E.g. metoprolol
(This is good for pts with asthma, as it spares beta-2 activity, which bronchodilates)


What extra effects does a non-specific beta-blocker (with alpha-1 antagonism) have vs. a more specific beta-blocker?
Example of such a drug?

More direct effects on blocking sodium retention.
Inhibition of vasoconstriction -> reduced SVR and BP.
Carvedilol does this.
(While this sound like in might be better for CHF, studies haven't shown superiority vs. drugs like metoprolol)


Do beta-blockers improve LVEF and help slow/prevent remodeling?



How can you directly target the vasoconstriction that contributes to HF?
(what's the connection to African Americans here?)

With a vasodilator such as isosorbide dinitrate/ hydralazine.
(Apparently African Americans tend not to respond to ACE inhibitors as well as other groups, but isosorbide dinitrate + hyralazine - "BiDil" works well instead. I don't think there's evidence that this combo doesn't work for other groups, though. Pharmacogenetics to more precisely predict who will respond would be nice here.)


What can you do to help LBBB from remodeling the heart?

Cardiac resynchronization therapy (CRT) aka a pacemaker.


How do you treat HF with preserved LVEF (HFpEF)?

This is less studied, and involves treating the underlying cause - usually HTN and diabetes.
Treatments for HFrEF are also used.