Pathophysiology of CHF I and II

Question 1

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

Answer 1

exercise intolerance

Question 2

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.

Answer 2

heart failure

Question 3

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

Answer 3

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

Question 4

Is heart failure acute or chronic?

Answer 4

either

Question 5

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

Answer 5

A

Question 6

What heart failure stage? prior or current symptoms

Answer 6

C

Question 7

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

Answer 7

B

Question 8

What heart failure stage? refractory

Answer 8

D

Question 9

What is the difference between heart failure stage and class?

Answer 9

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

Question 10

What heart failure class? symptoms at rest

Answer 10

4

Question 11

What heart failure class? symptoms with mild exertion

Answer 11

3

Question 12

What heart failure class? symptoms with strenuous exertion

Answer 12

2

Question 13

What heart failure class? asymptomatic

Answer 13

1

Question 14

Gender and heart failure?

Answer 14

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

Question 15

What is HFrEF?

Answer 15

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

Question 16

What is HFpEF?

Answer 16

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

Question 17

What is HFpEF borderline and improved

Answer 17

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

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

Question 18

What is the consequence of increasing preload in HF?

Answer 18

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

Question 19

What are the symptoms of volume overload in HF

Answer 19

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

Question 20

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

Answer 20

ventricular remodeling

Question 21

3 ways heart can respond to hemodynamic burden

Answer 21

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)

Question 22

What kind of hypertrophy? pressure overload

Answer 22

concentric

Question 23

What kind of hypertrophy? volume overload

Answer 23

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

Question 24

What is LVEF in concentric hypertrophy?

Answer 24

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

Question 25

What happens to the interpapillary distance in a dilated heart?

Answer 25

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

Question 26

What happens to conduction in those with a dilated heart?

Answer 26

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

Question 27

What are the effects of LBBB on ventricular function?

Answer 27

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

Question 28

What receptors are downregulated in situations involving cardiac dysfunction?

Answer 28

beta receptors --> abnormal myocyte function

Question 29

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

Answer 29

beta1, alpha1

Question 30

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

Answer 30

alpha1

Question 31

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?

Answer 31

beta1, beta2, alpha1

Question 32

Angiotensin II is a positive/negative inotrope.

Answer 32

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

Question 33

How does angiotensin ii potentiate fibroblast activity in the heart?

Answer 33

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

Question 34

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

Answer 34

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

Question 35

What is the prime directive of arginine vasopressin?

Answer 35

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

Question 36

How does the heart counter regulate the sympathetic inflow?

Answer 36

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

Question 37

What does ejection fraction have to do with BNP?

Answer 37

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

Question 38

What is the function of natriuretic peptides?

Answer 38

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

Question 39

3 ways to pharmacologically limit effects of AG II

Answer 39

1. ACE inhibitor 2. AR blocker 3. aldosterone antagonist

Question 40

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

Answer 40

T --> as measured by LV size and mass

Question 41

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

Answer 41

T --> better survival

Question 42

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

Answer 42

T --> better survival and fewer symptoms, better LVEF

Question 43

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

Answer 43

T --> better LVEF and survival

Question 44

Side effects of beta blockers

Answer 44

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

Question 45

Indications for CRT

Answer 45

symptomatic heart failure, LVEF150msec (LBBB)

Question 46

Short-term effects of CRT

Answer 46

increased LVEF, reduced LVEDD