Heart failure

Question 1

Define heart failure

Answer 1

-pathophysiologic state in which the heart is unable to pump blood at a rate commensurate with the body’s requirements, OR can do so only from an elevated filling pressure -has NOTHING to do with ejection fraction

Question 2

Main causes of heart failure

Answer 2

-Primary cardiac causes: ischemic heart disease is most common -HTN, DM, toxins (alcohol, adriamycin), thyrotoxicosis

Question 3

Syndrome of heart failure

Answer 3

-constellation of sxs including dyspnea, fatigue, exercise intolerance, swelling -can be acute or chronic

Question 4

Stages vs classes of heart failure. Which is preferred?

Answer 4

-stages: 1 = high risk pts without sxs (HTN, DM, CAD, fam history, cardiotoxic drugs), 2: structural heart disease (LVH, MI, low LVEF, dilation, valve dz) without sxs, 3: prior, current sxs 4. refractory (need LVAD or transplant) -classes I: asymptomatic, II sxs with moderate-strenuous exercise, III: with mild exertion IV at rest. -prefer the use of stages since they capture those without sxs but underlying structural dz

Question 5

Gender and survival differences in HF

Answer 5

-mean have more CVD at younger ages, but women over take them with age -women may have slight survival advantage -perhaps bc women have less compliance LV

Question 6

2 classifications of HF

Answer 6

1. heart failure with reduced LVEF (/50%: diastolic HF Note the definition of heart failure has nothing to do with EF, but this classification does

Question 7

Evolution of HF

Answer 7

Question 8

Myocardial failure is due to a ________________. There are several main physiological adjustments to stabolize or increase myocardial perforamce. Name 4.

Answer 8

• due to a specific acute or chronic insult to pump function
• increase preload, increased contractile elements, increased HR, increase contractility

Question 9

Why does the mechanism of increasing preload in heart failure turn into a bad idea?

Answer 9

-in severe LV dysfunction, the Frank-Starling curve has a peak, but then a downward portion at higher LV filling Ps. So with increased preload, eventually an increase in CO is not achieved. So blood pools in the heart, and raises LA pressure and can cause pulmonary congestion among other issues.

Question 10

Clinical correlations of increasing preload to a detrimental level in HF

Answer 10

• sxs of V overload: pulmonary congestion (cough, dyspnea, orthopnea, PND), visceral congestion (Liver, GI) leading to abdominal bloating, swelling, early satiety, anorexia, and peripheral edema can be seen.
• physical findings: JVD, HJR, peripheral edema, ascites, anasarca, displace diffuse apex, gallop rhythm

Question 11

Scenarios LV remodeling occurs in and what is the definition

Answer 11

• Many scenarios: HTN, acute MI, cardiomyopathy, valve dz, chronic ischemia
• process by which ventricular size, shape, and function are regulated by mechanical, neurohormonal, local, systemic, and genetic factors

Question 12

When the heart faces a hemodynamic burden, it can compensate in 3 general ways. name them and why they go wrong in HF

Answer 12

1. increase preload via Frank-Starling to increase cross-bridge formation, but this is limited and leads to dilatation
2. augment muscle mass to bear this extra load: remodeling and hypertrophy
3. recruit neurohormones to augment contractility: deleterious as chronic mechanism

Question 13

Which patterns of heart failure lead to systolic vs diastolic HF?

Answer 13

• concentric: diastolic HF; preserved EF
• eccentric: systolic HF; reduced EF–can also have mitral valve regurgitation due to change in ventricular structure

Question 14

Patients with myocardial disease due to ischemic heart disease or cardiomyopathy have an increased incidence of ________.

Answer 14

• Left bundle branch block
• makes things worse by altering timing for LV mechanical events

Question 15

Some effects and hemodynamic sequelae due to LBBB in heart disease

Answer 15

• delayed mitral and aortic valve opening and closing, prolonged LV isoV contraction time, loss of intra and interventricular synchrony, abnormal diastolic function
• results in reduced LVEF, paradoxical septal motion, reduced CO and MAP, increased LV filling rate and volume, increased duration of mitral regurgitation
• these lead to further remodeling and progression of dz

Question 16

T/F: There is evidence of genetic factors in HF.

Answer 16

-true, ultimately it is thought that genetically susceptible people undergo a “second hit” causing LV dysfunction.

Question 17

3 principal hemodynamic changes seen in HF that lead to neurohormonal activation.

Answer 17

1. increased ventricular wall stress
2. atrial HTN due to diastolic dysfunction, or fluid overload due to systolic dysfunction
3. reduced CO

Question 18

Overview of neurohormonal axis in HF

Answer 18

Question 19

Role of plasma NE levels in HF patients.

Answer 19

-patients with higher levels of NE died soon

Question 20

Clinical correlations of a patient with HF with an activated adrenergic system

Answer 20

• sxs: diaphoresis, anxiety, palpitations
• tachycardia, arrhythmias, initial increased inotropy, remodeling
• peripheral: cool, clammy extremities due to increased SVR

Question 21

What happens to the sensitivity to the adrenergic system over time in HF?

Answer 21

-patients become sensitized to B response and down regulate B receptors.

Question 22

Overview of RAAS system.

Answer 22

Question 23

Effects of AngII on heart, adrenal, brain, kidney, and vascular muscle

Answer 23

heart: positive inotrope/chronotropy; LV growth/LVH/remodeling
adrenal: aldosterone production and release

Brain: stimulates SNS, stimulate thirst and sodium appetite, release ADH, suppresses renin release, stimulates release of NE

Kidney: efferent and afferent arteriolar constriction, constrict mesangial cells, stimulates reabsorption of Na and bicarb

-VSMCs: hypertrophy, fibrosis and constriction (?)

Question 24

Aldosterone effects

Answer 24

• Na retention
• K and Mg loss
• myocardial and vascular fibrosis
• baroR dysfunction
• impairs arterial compliance
• prevent NE reuptake in myocardial cells (longer half life)
• regulates Na transport in colon, sweat, and salivary glands

Question 25

2 mechanisms causing secondary aldosteronism in CHF

Answer 25

1. increased production by zona glomerulosa due to increased Ang II
2. decreased rate of hepatic clearance due to reduced hepatic perfusion

Question 26

RAAS sxs in patients with HF

Answer 26

-pts complain of thirst, salt craving, volume overload signs, increased SVR, LVH/remodeling

Question 27

Main effects of ADH

Answer 27

• stimulated by AngII and baroRs; released from posterior pit.
• increases SVR and reduce clearance of water from kidney
• maintains volume to maintain output
• antagonist drugs available

Question 28

Role of cytokines in heart failure

Answer 28

• secreted in response to stress
• not felt to be causative but do contribute to progression by stimulating apoptosis or necrosis, progressive myocardial fibrosis, systemic effects of vasoconstriction (endothelin) and vasodepressor proinflammatory (TNFa and IL-6)

Question 29

Cytokine sxs in pts with HF

Answer 29

• fatigue, anorexia
• muscle wasting, cardiac cachexia, remodeling, anemia of chronic disease
• antagonist drugs showed poor outcomes

Question 30

T/F: despite all other issues, endothelial cells remain functional in HF

Answer 30

-false: likely many issues surrounding decrease in NO production and increase in vasoconstrictors and their effects

Question 31

Alterations in skeletal muscle in heart failure

Answer 31

• intrinsic abnormalities noted in skeletal muscle centering around metabolic alterations not related to hypoxia, but rather inadequare utilization by mitochondria
• impaired endurance due to reduced oxidative capacity
• decreased strength due to smaller muscle bundle CSA

Question 32

2 main factors leading to progression of HF, especially that of dilated cardiomyopathy.

Answer 32

-angiotenin II and NE: hypertrophy, apoptosis, ischemia, arrythmias, remodeling, fibrosis

Question 33

Ways the heart “fights back” against neurohormonal axis in heart failure

Answer 33

1. down regulating B receptors; physicians prescribe B-blockers to resensitive cells to positive effects, like increased inotropy.
2. ANP, BNP, CNP: oppose vasoconstrictive and salt and water retention of activated RAA and SNS

Question 34

Where does BNP come from, when, and what does it do?

Answer 34

• from ventricular myocardium distention (pressure overload and volume overload)–> vasodilation, Na excretion, decreased aldosterone levels
• levels correlation with progression of heart failure, marker for prognosis

Question 35

Prime directives of HF treatments

Answer 35

• improve survival
• improve sxs
• prevent progession by stage A prevent remodeling and B,C,D preventing or reversing remodeling.

Question 36

Types of treatments commonly used in reduced EF HF

Answer 36

1. beta blockers
2. ACEIs
3. ARBs
4. Aldosterone antagonist
5. vasodilators in AAs
6. Cardiac Resynchronization Therapy in LBBB

Question 37

Indications for CRT

Answer 37

-symptomatic heart failure

LVEF <35%

-QRS >150 msec

Question 38

Treatment of HF with preserved EF

Answer 38

• treat underlying condition
• treat HTN
• diuretics, ACEI, ARB as needed and sometimes B-blockers