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Cardiology > Pathophys. of CHF > Flashcards

Pathophys. of CHF Flashcards

1
Q

Is low LVEF used to diagnose heart failure?

A

No, but it is used to classify it.

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2
Q

Is exercise intolerance important in the diagnosis of heart failure?

A

Yep.

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3
Q

Definition of heart failure (HF)?

A

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

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4
Q

5 broad causes of heart failure?

A 
Primary (something wrong with heart itself: ischemia, inflammation, valves, etc.).
Hypertension
Diabetes
Toxins (EtOH, adriamycin)
Thyrotoxicosis
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5
Q

4 classic symptoms of HF?

A

Dyspnea, fatigue, exercise intolerance, and swelling.

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6
Q

What are stages A-D of HF?

A

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

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7
Q

What are NYHA classes I-IV of HF?

A

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

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8
Q

Gender-age relationship of CHF?

A

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

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9
Q

How does LV compliance vary between men and women?

A

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

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10
Q

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

A

LVEF < 40%.

This is also called “systolic HF,” because the problem is with getting blood out of the heart.

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11
Q

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

A

LVEF > 50% (thus 40-50% is borderline)

This is also called “diastolic HF,” because the main problem is with filling.

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12
Q

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

A

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

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13
Q

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

A 
Pulmonary congestion (cough, dyspnea, orthopnea, PND).
Visceral congestion (abdominal bloating, swelling, early satiety, anorexia).
Peripheral edema.
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14
Q

Review: Contrast concentric vs. eccentric hypertrophy.

A

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.

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15
Q

Why does dilated cardiomyopathy mess up heart valves?

A

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

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16
Q

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

A 
Delayed mitral and aortic opening/closure.
Prolonged LV isovolumetric contraction.
Loss of intraventricular synchrony.
Los of interventricular synchrony.
Abnormal diastolic function.
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17
Q

5 hemodynamic sequelae of the mechanical disruptions caused by LBBB?

A

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

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18
Q

3 principal hemodynamic changes in HF?

What is the “neurohormonal stimulation” of HF trying to accomplish?

A

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

Neurohormonal stimulation is trying to restore CO.

19
Q

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

A

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.

20
Q

How does circulating plasma NE in HF correlate with survival?

A

Higher NE, less survival.

21
Q

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

A

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

22
Q

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

A

Alpha-1

23
Q

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

A

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

24
Q

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

A

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.)

25
Q

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

A

It breaks down bradykinin.

26
Q

What effects does A-II have on kidneys?

On vasculature?

A

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

A-II causes hypertrophy of vascular smooth muscle.

27
Q

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

A

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

28
Q

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

A

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)

29
Q

Role of ADH aka. arginine vasopressin in HF?

A

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

30
Q

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

A

No. (it might help people feel better though)

31
Q

Several ways that endothelial dysfunction may contribute to HF?

A

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

32
Q

How does skeletal muscle tend to change?

A

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

33
Q

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

A

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.

34
Q

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

A 
The atria (and ventricles?) produce ANP and BNP, which oppose RAAS.
(recall that BNP is a useful marker of wall stress)
35
Q

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

A

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

36
Q

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

A

In length

37
Q

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

A

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

38
Q

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

A 
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
39
Q

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

Example of such a drug?

A

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)

40
Q

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?

A

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)

41
Q

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

A

Yep.

42
Q

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

A

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.)

43
Q

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

A

Cardiac resynchronization therapy (CRT) aka a pacemaker.

44
Q

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

A

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

Cardiology (46 decks)

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