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Cardio Week 2 > Lecture 19: Pathophysiology of Heart Failure, Understanding the Basis for Treatment > Flashcards

Lecture 19: Pathophysiology of Heart Failure, Understanding the Basis for Treatment Flashcards

1
Q

Which of the following is necessary to make the diagnosis of heart failure?

A

Symptoms of exercise intolerance

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2
Q

What is heart failure?

A
  1. The pathophysiologic state in which the heart is unable to pump blood at a rate commensurate with the body’s requirement OR
  2. can only do so from an elevated filling pressure
    The definition of heart failure has nothing to do with the ejection fraction
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3
Q

What are the causes of heart failure?

A 
Primary cardiac causes
	i. ischemic heart disease
	ii. myocardial disease
	iii. idiopathic dilated cardiomyopathy (DCM)
	iv. restrictive cardiomyopathy (RCM)
	v. hypertrophic cardiomyopathy (HCM)
	vi. inflammatory myocarditis
	vii. valvular heart disease
	viii. constrictive pericarditis
HTN
Diabetes
Toxins 
	i. alcohol
	ii. Adriamycin (which causes DCM)
Thyrotoxicosis
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4
Q

What is the syndrome of heart failure?

A 
Constellation of symptoms including 
	i. dyspnea
	ii. fatigue
	iii. exercise intolerance 
	iv. swelling
Can be acute OR chronic
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5
Q

What are the stages of heart failure?

A 
Stage A = high risk patients
	i. HTN
	ii. diabetes
	iii. family history
Stage B = structural heart disease
	i. LVH, MI, low LVEF
Stage C = prior or current symptoms
Stage D = refractory
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6
Q

What HF stage is symptomatic?

A

C

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7
Q

What are the classes of heart failure?

A

NYHA Classs
I = asymptomatic
II = Symptoms of heart failure with moderate/strenuous exertion
III = Symptoms of heart failure with mild exertion
IV = Symptoms of heart failure at rest

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8
Q

What are the gender and survival differences in heart failure?

A

From 0-74, men have higher prevalence of heart failure
From 75+, women have higher prevalence
Women tend to do better than men
Women have smaller volumes, higher pressure and have less compliance

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9
Q

What is the definition of impaired (reduced) LVEF?

A

Referred to as systolic heart failure
<40% of LVEF
HFrEF = heart failure with reduced ejection fraction

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10
Q

What is the definition of preserved LVEF?

A 
>50% Preserved LVEF
Referred to as DIASTOLIC HF
HFpEF (heart failure with preserved ejection fraction)
	i. HFpEF Border is 41-49%
	ii. HFpEF improved is >40%
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11
Q

Does the definition of heart failure have something to do with ejection fraction?

A

NO only the classification does

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12
Q

What is the prime directive for compensatory pathophysiologic mechanisms in heart failure?

A

To restore cardiac output regardless of the expense

RESTORE CO NINJAAA

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13
Q

When there is myocardial failure, what are the adjustments the heart makes to stabilize or increase myocardial performance?

A
  1. Increased preload
  2. Increased contractile elements
  3. Increased heart rate
  4. Increased state of contractility
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14
Q

What happens to the Frank-Starling relationship of patient with heart failure?

A

It shifts down and to the right
Which means not enough force is generated per
Increase in length

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15
Q

What are symptoms due to volume overload?

A
  1. pulmonary congestion (cough, orthopnea, PND)
  2. Visceral congestion (ascites)
  3. Peripheral edema
  4. anasarca
  5. diffuse apex
  6. JVD (jugular venous distension)
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16
Q

What is anasarca?

A

Known as generalized extreme edema
Characterized by widespread swelling of the skin due to effusion of fluid into the extracellular space
Caused by anything that can lead to interstitial fluid build up

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17
Q

When does LV remodeling happen?

A

Process by which ventricular size, shape and function are regulated by other factors

  1. HTN
  2. Acute myocardial infarction
  3. Cardiomyopathy (DCM, HCM, RCM)
  4. Valvular heart disease
  5. Chronic ischemia
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18
Q

What is the heart’s response to hemodynamic burden (like volume overload)?

A
  1. Use Frank-starling mechanism to increase cross-bridge formation
  2. augment muscle mass to bear extra load
  3. recruit neurohormones to augment contractility
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19
Q

What is relative wall thickness?

A

Determines whether hypertrophy will be concentric or eccentric
If wall thickness is higher than 0.45, you have concentric wall thickness
If wall thickness is lower than 0.34 then you have eccentric wall thickness

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20
Q

What are the three responses to LV dysfunction?

A
  1. LV remodeling (hypertrophy or dilatation)
  2. Neurohormonal stimulation
    i. Sympathetic nervous system
    ii. RAAS
  3. Vasoconstriction of arterioles
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21
Q

What are the characteristics of eccentric hypertrophy?

A

Due to VOLUME overload
Same RWT but wall stress is not corrected to normal
Sarcomeres are added in series so you get stretching of muscle
Sarcomeres that are added are ABNORMAL

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22
Q

How do LV and RV get remodeled during congestive heart failure?

A 
They hypertrophy (and they can do so either concentrically or eccentrically; former is pressure overload, latter is volume overload)
If RV is remodeled, eccentric/concentric terminology not used
RV remodeling is NOT mentioned in heart failure because it has nothing to do with ejection fraction
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23
Q

What are the key characteristics of concentric hypertrophy?

A

In response to pressure overload
-parallel addition of sarcomeres caused increased myocyte width, which in turn increases wall thickness
Increase in RWT because chamber radius does not change

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24
Q

What type of remodeling leads to HFrEF?

A

Heart failure with reduced ejection fraction
Eccentric hypertrophy
Ejection fraction is reduced because added sarcomeres are contracting abnormally

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25
Q

What type of remodeling leads to HFpEF?

A

Heart failure with preserved ejection fraction
Concentric hypertrophy
Ejection fraction is preserved (but ESV and EDV are both decreased)

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26
Q

What is ejection fraction?

A

EDV-ESV/EDV
So if you get an equal reduction in both ESV and EDV, you can still get a preserved ejection fraction while still being in heart failure
-concentric hypertrophy

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27
Q

What happens to the chordae tendinae in eccentric hypertrophy of the ventricle?

A

You get mitral/tricuspid regurgitation because the valve leaflets are pulled farther and farther apart since circle is expanding into basketball

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28
Q

What is the effect of LBBB on ECG?

A

Longer QRS complex
QRS duration = 160ms
On V1, you can also see a wide and deep inverted S wave

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29
Q

What are the ECG changes in patients with h myocardial disease?

A
  1. patients with cardiac ischemia or cardiomyopathy have increased LBBB ranging from 27-54%
  2. LBBB alters the sequence of left ventricular activation thereby affecting mechanical events of the cardiac cycle and resulting hemodynamics
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30
Q

What are the symptoms of LBBB on ventricular function?

A
  1. delayed mitral and aortic valve opening and closure
  2. prolonging of left ventricular isovolumic contraction time
  3. Loss of intraventricular synchrony
  4. loss of interventricular synchrony (between LV and RV)
  5. abnormal diastolic function
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31
Q

What are the hemodynamic effects of LBBB? Consequences?

A

Delays in contraction time leads to
i. reduced LVEF
ii. paradoxical septal motion
iii. reduced CO and reduced MAP
iv. increased LV filling rate and volume
v. increased duration of MR
Leads to further remodeling and progression of disease

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32
Q

What are the principal hemodynamic changes in patients with heart failure?

A
  1. increased ventricular wall stress
  2. atrial hypertension due to diastolic dysfunction, fluid overload
  3. reduced cardiac output
    Prime directive is to restore cardiac output!
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33
Q

What is the benefit of neurohormonal on heart failure?

A

Works very well for self-limited, short-term responses
NOT long-term chronic diseases
Because we didn’t used to live this long

34
Q

What are the neurohormonal pathways activated in heart failure?

A
  1. RAAS (renin-angiotensin-aldosterone system)
  2. Sympathetic nervous system activation
    -SNS is whats initially activated in heart failure
    -increases HR and contractility (but can lead to hypertrophy and injury)
    -increases vasoconstriction
    Long-term neurohormonal pathways leads to disease progression!
35
Q

What do the plasma NE levels in heart failure indicate?

A

The higher the NE levels, the greater the mortality risk

36
Q

What is the MoA of sympathetic nervous system on myocardial beta receptors?

A

Gstimulating protein

Leads to higher HR and contractility

37
Q

What happens to the SNS response in patients with cardiomyopathy?

A

Beta receptors are not working normally
If you overstimulate the B receptors, they start to downregulate
That’s why SNS can lead to dysfunction, chronic stimulation leads to downregulation which means not enough CO when you need it!

38
Q

What are the symptoms of sysmpathetic overload?

A
  1. diaphoresis
  2. anxious
  3. palpitations
  4. tachycardia
  5. arrhythmias
  6. cool, clammy extremities
  7. Increased SVR
39
Q

What is the renin-angiotensin-bradykinin system?

A

When renin is activated, leads to Angiotensin II which
i. increases aldosterone release and fluid retention
ii. increases calcium current to promote vasoconstriction
iii. augments sympathetic activation
iv. ULTIMATELY you get increased BP
ACE also degrades bradykinin

40
Q

What is the role of bradykinin?

A

Stimulates production of prostaglandins which in turn lead to vasoDILATION
Is degraded by ACE

41
Q

What is the relationship between bradykinin and ACE?

A

ACE degrades bradykinin (thereby having two roles in promoting vasoconstriction)

42
Q

What does angiotensin II act on?

A
  1. heart
  2. adrenal
  3. brain
  4. Kidneys
  5. vasculature
43
Q

What does angiotensin II do for the heart?

A
  1. positive inotrope and chronotrope
  2. LV growth/hypert rophy/remodeling if activated chronically
  3. leads to decrease in compliance due to INCREASE in interstitial fibrosis
44
Q

How does angio II affect the brain?

A
  1. Potentiates SNS
  2. stimulates thirst and sodium appetite
  3. Increases ADH release
  4. Suppresses renin release (feedback inhibition)
  5. Increases NE release
45
Q

How does angio II affect the kidney?

A
  1. Constricts afferent and efferent vasculature
  2. Contricts mesangial cells (SMCs in kidney)
  3. Stimulates proximal tubular reabsorption of Na and HCO3-
46
Q

How does angio II affect the vasculature?

A

Hypertrophy of the smooth muscle

47
Q

What are mesangial cells?

A

Specialized cells around blood vessels in the kidney
Specialized smooth muscle cells that regulate blood flow through the capillaries
Divided into
I. extraglomerular mesangial cells
II. intraglomerular mesangial cells

48
Q

What is the pathophysiology of interstitial fibrosis as caused by angio II?

A

Two methods
1. Angio II + Angio II receptor = increase in Calcium signals = upregulation in genes for collagen
2. Aldosterone (stimulated by angio II) leads to upregulation of genes for collagen
Collagen = interstitial fibrosis
This is what happens in the HEART

49
Q

What is the role of aldosterone?

A
  1. sodium retention
  2. potassium and magnesium loss
  3. myocardial and vascular fibrosis
  4. baroreceptor dysfunction
  5. impairs arterial compliance (fibrotic deposition)
  6. prevention of myocardial NE uptake
50
Q

What are two pathophysiologic mechanisms of secondary aldosteronism in CHF?

A
  1. increased production by zona glomerulosa?
    • due to increased angiotensin stimulation
  2. decreased rate of hepatic clearance of aldosterone
51
Q

What are the symptoms of heart failure in relation to the RAA system?

A

Patients complain of thirst and salt craving
Volume overload
Increased SVR and LV hypertrophy

52
Q

What are the key characteristics of arginine vasopressin?

A

Angiotensin 2 stimulates ADH release
Increases SVR
Reduces water clearance from kidney

53
Q

What are the roles of cytokines in heart failure?

A

Not felt to be causative but does contribute to progression

  1. Stimulates apoptosis or necrosis
  2. stimulates myocardial fibrosis
54
Q

What are the symptoms of heart failure that correlate with cytokines?

A
  1. muscle wasting
  2. cardiac cachexia
  3. remodeling
  4. fatigue
  5. anorexia
55
Q

What is the role of endothelial dysfunction in heart failure?

A
  1. increased cytokine levels imparing EDRF synthesis (NO)
    -EDRF = endothelium derived relaxing factor
  2. Increased ACE activity = increased bradykinin breakdown
  3. Oxygen radicals inactivating NO
  4. Chroncally reduced blood flow with decreased NO synthase
  5. increased endothelial dependent vasoconstrictors like endothelin
    Basically you are losing the endothelial cytokines that can vasodilate your vessels for you
56
Q

What do you need to do hemodynamically to improve symptoms?

A

Vasodilate and growth inhibiting cytokines are upregulatd
Vasoconstricting and growth promoting = worsening symptoms because of progressive remodeling
In CHF, vasoconstrictors > vasodilators

57
Q

What is the relationship between skeletal muscle and heart failure?

A
  1. Intrinsic abnormalities noted in skeletal muscle
  2. Metabolic alterations due to inadequate oxygen utilization by mitochondria
    • not related to tissue hypoxia
  3. Impaired endurance due to reduced oxidative capacity
  4. Decreased strength due to smaller muscle bundle cross-sectional area
58
Q

How does neurohormonal activation lead to downfall of the patient?

A

Neurohormonal activation = Angiotensin II + Norepinephrine

i. Hypertrophy
ii. Apoptosis
iii. Ischemia
iv. Arrhythmias
v. Remodeling 
vi. Fibrosis
59
Q

What does the heart do to counteract cardiomyopathy?

A
  1. Decrease in number and function of beta receptors (to neutralize their efficacy and downregulate SNS effect)
  2. Decrease in ATP consumption to save energy
    -this prevents calcium from coming to
    Decrease contractility
  3. ANP and BNP (counterregulatory hormones)
60
Q

What are the key characteristics of ANP and BNP?

A

Both are part of the hearts counterregulatory system in response to ischemia
Opposes vasoconstrictive and salt/water retention of activated RAA and sympathetic function

61
Q

What are the characteristics of B-type Natriuretic Peptide (BNP)?

A
  1. Causes
    i. vasodilation
    ii. promotes sodium excretion
    iii. decreases aldosterone levels
    iv. inhibits RAAS
  2. Found in cardiac ventricles
  3. Activated by:
    i. myocardial stretch in ventricles
    ii. volume expansion
    iii. pressure overload
  4. BNP levels are related to LVend-diastolic pressure
62
Q

Which of the following is characteristic of eccentric hypertrophy?

A

Increased myocyte length

63
Q

What is the prime directive of compensatory mechanisms of heart?

A

Restore cardiac output!

64
Q

What is the prime directive of treatment?

A

Prevent or reverse disease progression
For stage A = prevent remodeling
For stage B-D = delay or reverse remodeling

65
Q

What are ways to inhibit angiotensin action (RAA system)?

A
  1. ACE inhibtors
  2. ARBs (ACE receptor blocker)
  3. Aldosterone receptor antagonist
66
Q

What is the first line therapy for systolic heart failure (reduced ejection failure)?

A
  1. beta blockers
    i. Beta 1 selective blockers
  2. ACE inhibitors
67
Q

What are the downfalls of ACE inhibition alone?

A

Angiotensin 2 is only half of the equation for disease progression (the other side is increased norepinephrine)

68
Q

How does inhibiting aldosterone aid congestive heart failure patients?

A

Less Na retention
Less myocardial/vascular effects
Limits potassium loss
Spironolactone group had great survivability for Class III and IV heart failure patients (those with symptoms already)

69
Q

What is an example of an ACE inhibitor?

A

Enalapril

-decreases heart size increase and also decreases EDV

70
Q

What are examples of Aldosterone receptor inhibitor?

A
  1. spironolactone
  2. Eplerenone
    Used for class III and IV heart
    Failure patients
71
Q

What are the beta1 selective blockers?

A

Metoprolol

72
Q

Why don’t you want to use a non-selective beta blockers?

A

Because beta 2 is a bronchodilator

73
Q

What is metoprolol?

A

A selective beta 1 blocker

74
Q

What is the relationship between LVEF and beta-blockers?

A

Taking beta blockers increase the level of LVEF, thereby counteracting the effects of myocyte remodeling
Beta blockers are used to increase LVEF to prevent the downregulation of the beta receptors on the heart
-remember, beta receptors are downregulated when there is chronic SNS stimulation, so patients have reduced cardiac output when needed
-therefore, giving beta blockers will prevent this downregulation and allow patients to better respond to acute SNS stimulation when the body needs it

75
Q

Why does vasoconstriction occur in patients with LV dysfunction?

A

Because of angiotensin II release in order to preserve BP since there is a decreased EF and decreased CO
Therefore, increasing vasodilation = decreasing afterload = increasing EF and CO

76
Q

What is the relationship between vasodilators and heart failure patients?

A

Greater survivability because vasodilation = decrease afterload

77
Q

What are the primary targets of treatment in heart failure?

A
  1. beta blockers
  2. ACE inhibitors, ARBs, aldosterone antagonists (all first line)
  3. digoxin/inotropes
  4. diuretics
  5. Cardiac resynchronization therapy
78
Q

What does CRT mean? Significance?

A

Cardiac resynchronization therapy
Shrinks the heart size
And increases LVEF

79
Q

What are the indications of CRT?

A
  1. symptomatic heart failure

2. LVEF 150ms

80
Q

What is the treatment of HF with preserved LVEF?

A
  1. Treat underlying condition
  2. Treat hypertension
  3. Diuretics as needed
  4. ACE inhibitor or ARB
  5. Beta-blockers in some cases
    Only one study on which to base treatment
    Hard to treat
81
Q

What is the classic presentation of HFpEF?

A

Old woman with HTN and shortness of breath

82
Q

What is Nesiritide?

A

A recombinant BNP medication
Given to increase sodium and fluid excretion
Counteracts the RAAS system

Cardio Week 2 (11 decks)

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