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CVPR > CVPR Week 9: Heart Failure > Flashcards

CVPR Week 9: Heart Failure Flashcards

1
Q

Objectives

A
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2
Q

Heart failure definition

A
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3
Q

Heart failure epidemiology

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4
Q

Causes of heart failure results in disorders of?

6 listed

A
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5
Q

What are cardiomyopathies?

A
  • diseases or conditions that affect the myocardium
  • can lead to LV dysfunction and possibly heart failure
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6
Q

Cardiomyopathy types

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7
Q

Causes of heart failure

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8
Q

Assessment of function of heart

A
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9
Q

What is the first test to evaluate heart failure?

A

Echocardiography

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10
Q

EF AKA

A

Ejection fraction

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11
Q

EF description

A

percentage of blood volume in the ventricle pumped out with each beat

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12
Q

EF =

A

LVEDV - LVESV

LVEDV

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13
Q

Echocardiography

A
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14
Q

Types of heart failure

A
  • heart failure w/ reduced ejection fraction
  • heart failure w/ preserved ejection fraction
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15
Q

What is systolic HF?

A

systolic heart failure

HF with Left Ventricular (LV) ejection fraction (LVEF) <= 40%

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16
Q

What is diastolic HF

A

diastolic heart failure is Heart failure with a preserved ejection fraction

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17
Q

Diastolic HF =

A

LV EF >= 50%

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18
Q

Borderline diastolic HF =

A

LVEF 41 - 49%

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19
Q

Systolic HF =

A

LVEF <= 40%

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20
Q

Prevalence of diastolic HF =

A

~50%

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21
Q

Heart failure types and ejection fraction equations

A
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22
Q

Pathophysiology of heart failure

A
  • an index event damages the heart muscle and produces a decline in the pumping capacity of the heart (LV dysfunction)
  • Neurohumoral systems are activated
  • Initially this increased activity maintains perfusion of vital organs and systems attempt to compensate for the damage of the index event but with time damage the heart
  • Heart failure progresses as a result of the overexpression of these systems
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23
Q
A
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24
Q

Neurohumoral systems that attempt to compensate for heart failure

A
  • Sympathetic nervous system
  • Renin-Angiotensin-Aldosterone-System
  • Vasopressin release
  • Cytokine release
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25
The pathways of pathology in heart failure
26
Deleterious neurohormones involved with the pathogenesis of heart failure
* increased preload (increased volume) and afterload (increased pressure) * sodium and water retention * vasoconstriction * Impaired diastolic and systolic function * myocyte hypertrophy and myocardial fibrosis * These lead to ventricle remodeling and eventually cell death
27
Ventricular remodeling occurs in heart failure as a response to?
Increased preload and afterload (increased volume and pressures) from sodium and water retention as well as vasoconstriction causes ventricular hypertrophy and cell death These changes in myocardial size and shape are associated with cell death
28
What is the result of ventricular remodeling in heart failure?
These changes in myocardial size and shape are associated with cell death
29
Why does cell death occur in heart failure?
the conditions and ventricular remodeling that takes place causes a cycle of increased stress leading to further acceleration of cell death and fibrosis
30
Describe how the sympathetic nervous system is involved in the pathophysiology of heart failure
sympathetic activation initially helps to maintain cardiac output The initial increase in NE levels causes * increased cardiac contractility * increased heart rate * helps maintain the glomerular filtration rate The long-term increase in NE levels causes * Increased afterload (vasoconstriction) * Fibrosis * Arrhythmias
31
The long-term increase in NE levels from sympathetic activation in heart failure causes
* Increased afterload (vasoconstriction) * Fibrosis * Arrhythmia
32
The initial increase in NE levels from sympathetic activation in heart failure causes
* increased cardiac contractility * increased heart rate * helps maintain the glomerular filtration rate
33
Describe the role of the RAAS in heart failure pathophysiology
Poor cardiac output causes reduced renal perfusion which stimulates renin release The increased renin produces angiotensin II which causes * efferent glomerular arteriolar vasoconstriction * vasoconstriction * increases aldosterone synthesis which causes * more Na+ reabsorption and K+ excretion The overall effect results in an increased afterload leading to further reduction in cardiac output and even worse renal perfusion and increased preload due to the Na+ and water retention
34
Describe the role of vasopressin iin heart failure
Vasopressin is released from the posterior pituitary gland which is a potent vasoconstrictor causing increased afterload and also it promotes water reabsorption in the renal tubules
35
Describe the role of endothelial cells in the pathophysiology of heart failure
endothelial cells release cytokines in response to injury interleukins and tumor necrosis factor cause * myocyte hypertrophy and apoptosis * Decreased contractility/inotropy * oxidative stress Endothelin causes * Vasoconstriction * collagen deposition -\> fibrosis -\> less compliant ventricle
36
Interleukins and tumor necrosis factor in the pathophysiology of heart failure
released from endothelial cells and causes * myocyte hypertrophy and apoptosis * decreased contractility/inotropy * oxidative stress
37
Endothelin in the pathophysiology of heart failure
released from endothelial cells and causes * vasoconstriction * collagen deposition -\> fibrosis -\> less compliant ventricle
38
Describe the changes involved in LV remodeling in response to heart failure
39
What is this?
myocyte hypertrophy and apoptosis and ECM degradation from LV remodeling in heart failure
40
What is this?
ventricular fibrosis
41
What is this?
mitral valve regurgitation in response to LV remodeling from heart failure
42
Non-deleterious hormones of heart failure
Myocardial release of B-type natriuretic peptide (BNP) * beneficial * ventricular in origin * vasodilation and natriuresis * decrease preload and afterload * MArker for myocardial stretch
43
Summary of heart failure pathophysiology
44
How is heart failure Dx?
45
What does heart failure look like?
46
Cardinal manifestations of HF
* Dyspnea on exertion (DOE) - shortness (dyspnea) and fatigue causing exercise intolerance * Salt and water retention leading to congestion
47
48
What is congestion in heart failure due to?
congestion is due to increased filling pressures from * increased preload (increased volume) * salt and water retention * Increased afterload (increased pressure) * Left-sided filling pressure = pressure in the LV at the end diastole (LVEDP) * Right-sided filling pressure = pressure in the RV at the end of diastole (RVEDP)
49
What are the types of congestion?
pulmonary and systemic
50
What causes pulmonary congestion?
arises from increased left heart filling pressures (LVEDP)
51
What causes systemic congestion?
arises from increased right heart filling pressures (RVEDP) The most common cause of right-sided filling pressures is elevated left-sided filling pressures
52
The most common cause of right-sided filling pressures?
elevated left-sided filling pressures
53
Symptoms of pulmonary congestion 4 listed
54
Symptoms of systemic congestion 5 listed
55
Physical exam findings of pulmonary congestion
* Inspiratory crackles on lung exam * Decreased breath sounds from pleural effusion
56
Physical exam findings of systemic congestion 6 listed
* Left and/or right sided S3 (rapid early filling) * Mitral and/or tricuspid valve regurgitation murmur * Jugular venous distention (JVD) * Distended abdomen * Enlarged liver * Edema
57
Stages of heart failure
A-D
58
Heart failure Stage A
At high risk for HF but without structural heart disease or symptoms of HF * HTN * DM * CAD * obesity * metabolic syndrome * Hx of familial cardiomyopathy * cardiotoxin exposure
59
Heart failure Stage B
Structural heart disease but without previous signs or symptoms of HF * LV hypertrophy * LV dilation * MI * asymptomatic valvular disease
60
Heart failure Stage C
Structural heart disease with current or previous signs or symptoms of HF
61
Heart failure Stage D
Refractory HF requiring specialized interventions * Mechanical circulatory support * transplant * hospice
62
NYHA HF classification system
63
What is his stage of HF and NYHA class?
64
Why can't he lie flat?
65
What are his signs and symptoms of congestion?
66
Why is his HR and BP elevated?
67
What components suggest LV remodeling
68
What can be done to help his symptoms and improve his condition?
69
What are the goals of therapy in treating HF?
70
Therapeutic interventions that affect the abnormal activation of what systems to treat HF?
* Sympathetic system * RAAS * Vasopressin release * Cytokine release
71
Important interventions targeted at treating HF
* abnormally activated systems * improve the abnormal elevations n preload and afterload * reduce fibrosis * revere remodeling
72
Treatments to improve symptoms and quality of life
73
HF treatments to reduce hospitalizations
74
Treatments of HF to improve survival
75
Treatments of HF to reverse LV remodeling
76
ARNI AKA
angiotensin-neprilysin inhibition
77
Not reviewed
78
What is her stage and NYHA class?
79
What is the likely etiology of her HF/LV dysfunction?
80
What can be done to help her symptoms and improve his condition?
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CVPR (93 decks)

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