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Cardiology > Pathophysiology of CHF I and II > Flashcards

Pathophysiology of CHF I and II Flashcards

1
Q

What is necessary to make the diagnosis of heart failure: low left ventricular ejection fraction, symptoms of exercise intolerance, presence of heart murmur

A

exercise intolerance

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2
Q

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.

A

heart failure

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3
Q

What does the definition of heart failure have to do with left ventricular ejection fraction?

A

NOTHING –> you can classify HF on basis of LVEF but LVEF function doesn’t define HF

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4
Q

Is heart failure acute or chronic?

A

either

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5
Q

What heart failure stage? high risk patients (htn, diabetes, coronary disease, family history, cardiotoxic drugs)

A

A

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6
Q

What heart failure stage? prior or current symptoms

A

C

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7
Q

What heart failure stage? structural heart disease (LVH, MI, low LVEF, dilatation, valvular disease)

A

B

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8
Q

What heart failure stage? refractory

A

D

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9
Q

What is the difference between heart failure stage and class?

A

classes have to do with categorizing symptoms once you have them, stages have to do with estimating prognosis

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10
Q

What heart failure class? symptoms at rest

A

4

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11
Q

What heart failure class? symptoms with mild exertion

A

3

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12
Q

What heart failure class? symptoms with strenuous exertion

A

2

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13
Q

What heart failure class? asymptomatic

A

1

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14
Q

Gender and heart failure?

A

men get it early, women overtake by 75. women do better.

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15
Q

What is HFrEF?

A

heart failure with reduced ejection fraction (<=40%) AKA systolic HF

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16
Q

What is HFpEF?

A

heart failure with preserved LVEF (>=50%) AKA diastolic HF

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17
Q

What is HFpEF borderline and improved

A

HFpEF, borderline = heart failure with 41-49% LVEF

HFpEF, improved = heart failure with >40% LVEF but used to be lower

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18
Q

What is the consequence of increasing preload in HF?

A

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

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19
Q

What are the symptoms of volume overload in HF

A

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

20
Q

Process by which ventricular size, shape, and function are regulated by mechanical, neurohormonal, local, systemic, and genetic factors.

A

ventricular remodeling

21
Q

3 ways heart can respond to hemodynamic burden

A
  1. use starling mechanism/preload to increase cross bridge formation (limited and leads to dilatation)
  2. augment muscle mass (remodeling and hypertrophy)
  3. recruit hormones to augment contractility (deleterious if used chronically)
22
Q

What kind of hypertrophy? pressure overload

A

concentric

23
Q

What kind of hypertrophy? volume overload

A

eccentric –> think about a balloon filling up causing the heart to get bigger w/o making wall thicker

24
Q

What is LVEF in concentric hypertrophy?

A

usually normal –> pressures are higher but heart is stronger so don’t really affect ejection fraction –> but still have congestion, etc.

25
Q

What happens to the interpapillary distance in a dilated heart?

A

increases –> also stretch annulus of valve –> leads to mitral valve regurgitation

26
Q

What happens to conduction in those with a dilated heart?

A

have increased incidence of left bundle branch block leading to QRS elongation

27
Q

What are the effects of LBBB on ventricular function?

A
  1. delayed mitral/aortic valve opening/closure
  2. prolongation of left ventricular isovolumic contraction time
  3. loss of interventricular syncrhony
  4. abnormal diastolic function
  5. paradoxical septal motion
    etc. etc –> leads to further remodeling/progression of disease
28
Q

What receptors are downregulated in situations involving cardiac dysfunction?

A

beta receptors –> abnormal myocyte function

29
Q

What receptors are implicated in increased renal sympathetic activity in heart failure that contribute to sodium retention, activation of RAS, and ultimately, disease progression?

A

beta1, alpha1

30
Q

What receptors are implicated in increased vascular constriction in heart failure and ultimately, disease progression?

A

alpha1

31
Q

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?

A

beta1, beta2, alpha1

32
Q

Angiotensin II is a positive/negative inotrope.

A

positive –> leads to LV growth, hypertrophy, remodeling in the long term

33
Q

How does angiotensin ii potentiate fibroblast activity in the heart?

A

ag II –> IP3/PKC –> calcium + aldosterone –> corticoid receptor = genes for collagen/interstitial fibrosis

34
Q

What are the two mechanisms by which secondary aldosteronism occurs in CHF?

A
  1. increased ZG production due to increased plasma angiotensin stimulation
  2. decreased hepatic clearance b/c of reduce hepatic perfusion
35
Q

What is the prime directive of arginine vasopressin?

A

maintain volume to maintain CO (via increasing SVR and reducing free water clearance in kidney)

36
Q

How does the heart counter regulate the sympathetic inflow?

A
  1. reduce beta receptors
  2. increase inhibitory g protein
  3. reduce atp stores to prevent cAMP from allowing inflow of calcium
  4. counter regulatory natriuretic peptides
37
Q

What does ejection fraction have to do with BNP?

A

nothing –> BNP is related to wall stress (LVEDP)

38
Q

What is the function of natriuretic peptides?

A

oppose vasoconstrictive and salt/water retention of activated RAS and sympathetic system

39
Q

3 ways to pharmacologically limit effects of AG II

A
  1. ACE inhibitor
  2. AR blocker
  3. aldosterone antagonist
40
Q

T/F the use of ACE-I and ARBs can reduce disease progression in CHF

A

T –> as measured by LV size and mass

41
Q

T/F the use of aldosterone antagonists can reduce disease progression in CHF

A

T –> better survival

42
Q

T/F the use of beta1 selective blockers can reduce disease progression in CHF

A

T –> better survival and fewer symptoms, better LVEF

43
Q

T/F the use of combined beta/alpha blockers can reduce disease progression in CHF

A

T –> better LVEF and survival

44
Q

Side effects of beta blockers

A

fatigue and low bp –> have to scale the dose up slowly

45
Q

Indications for CRT

A

symptomatic heart failure, LVEF150msec (LBBB)

46
Q

Short-term effects of CRT

A

increased LVEF, reduced LVEDD

Cardiology (41 decks)

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