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CV > Heart Failure: General > Flashcards

Heart Failure: General Flashcards

1
Q

Define Heart Failure

A
  1. Clinical syndrome (collection of signs and symptoms)
    - results when heart cannot pump enough blood while maintaining normal pressures in the heart chambers and lung vessels
  2. Chronic dz from injury to heart
    - ->compensatory changes in cardiac structure and function
  3. Fastest growing heart disease
    - Disease of aging + all the lives we’ve saved from MIs & other heart issues
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2
Q

Heart Failure Prevention

A

There is no cure.

More aggressive treatment of hypertension and atherosclerotic disease

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3
Q

Types of Heart Failure

A
  1. Systolic Heart Failure (HFrEF): contractile function of the heart is impaired
  2. Heart Failure with Preserved Ejection Fraction (HFpEF): abnormalities in myocardial relaxation, stiffness
    - less compliant LV
    - affects elderly

*Same clinical syndrome results

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4
Q

Causes of HF: General

A

Any abnormality of the heart can cause clinical heart failure

“The Final Common Pathway”

Issues with:
Muscle
Valves
Electrical system Blood vessels Pericardium

General causes:

  • Inflammatory HD
  • Extracardial Cardiomyopathy
  • Secondary Cardiomyopathy
  • Idiopathic Cardiomyopathy (40%)
  • Pericardial Disease
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5
Q

Causes of HF: Inflammatory Heart Disease

A 
▫ Infectious (Lyme, HIV) 
▫ Myocarditis 
▫ Sarcoidosis
▫ Peripartum
▫ Hypersensitivity
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6
Q

Causes of HF: Extramyocardial Cardiomyopathy

A

*not intrinsic to the muscle itself

▫ CAD
▫ Congenital
▫ Valvular
▫ Hypertension

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7
Q

Causes of HF: Secondary Cardiomyopathy

A 
▫ Inherited
▫ Nutritional
▫ Amyloidosis
▫ Metabolic
▫ Rheumatologic
▫ Toxic
▫ Hemochromatosis
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8
Q

Most common etiologies of HF

A

Most patients have CAD, HTN, or both

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9
Q

What are HF symptoms mostly due to?

A

Retention of salt and fluid causing increase in intra- and extravascular fluid…thus “congestive” HF

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10
Q

What are HF signs mostly due to?

A

Reflection of cardiac filling pressure and perfusion

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11
Q

Symptoms of Fluid overload

A
  • Respiratory Distress (due to high LA pressure)
  • Reduced exercise capacity
--These reflect high CVP-- 
• Edema
• Anorexia
• Abdominal Bloating
• Early Satiety
• Abdominal discomfort
• Cachexia
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12
Q

Left Sided Heart Failure Symptoms:

A
  1. Respiratory Distress (due to high LA pressure)
    􏰂 • Exertional dyspnea
    􏰂 • Wheezing-bronchospasm due to peri-bronchiolar edema
    􏰂 • Orthopnea
    􏰂 • Nocturnal cough
    􏰂 • Paroxysmal nocturnal dyspnea (PND)
    􏰂 • Dyspnea at rest
  2. Reduced exercise capacity
    (classic for HF)
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13
Q

Right Sided HF

A
  • Due to increased CVP
  • Most common cause is LHF thus most patients will also present with LHF symptoms and signs
  • Leads to congestion of the liver
  • Edema
  • Anorexia
  • Abdominal Bloating
  • Early Satiety
  • Abdominal discomfort
  • Cachexia
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14
Q

Orthopnea

A

*Congestive (Left) HF

• supine–>increased venous return–>heart can’t adapt
–>increased LA filling P
–>pulmonary venous HTN –> increased PCWP–>
edema–>dyspnea

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15
Q

PND

A

Paroxysmal Nocturnal dyspnea

Similar to orthopnea

Wake up acutely short of breath, relieved by sitting up

In HF, may be caused by critical increase in pulmonary capillary pressure

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16
Q

Cardia Cachexia

A
  • Severe weight loss due to loss of appetite & malabsorption that comes with liver congestion and gut edema
  • Combined w/catabolic state that results from neurohormonal alterations in HF
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17
Q

Symptoms of Impaired perfusion

A
  • Usually only very severe cases
  • Most pts only present with congestion
  • Fatigue
  • Weakness (muscle breakdown)
  • Anorexia
  • Confusion
  • Impaired cognition
  • renal insufficiency
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18
Q

Why is HF difficult to dx?

A

Because Fluid Overload is hard to detect:

• Symptoms tend to progress insidiously

• Patients gradually limit activity to
minimize symptoms

• They often present with advanced symptoms but subtle signs when compensatory mechanisms fail

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19
Q

General symptoms for HF in general

A
  1. Respiratory Distress:
    - DOE
    - Wheezing
    - Orthopnea
    - PND
    - Dyspnea at rest
  2. Reduced Exercise Capacity
  3. Fatigue
  4. Weakness
  5. Abdominal Discomfort
  6. Bloating
  7. Early satiety
  8. Anorexia
  9. Confusion
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20
Q

What are signs of volume overload?

A 
• Elevated neck veins 
• Hepatomegaly
• Ascites--severe HF
• Edema-- in order to link edema to HF, need to know CVP
• Hepatojugular reflux
• Rales (crackles) in lungs
-transudation into alveolar space
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21
Q

Hepatojugular Reflex

A

• Key sign! If JVP increases and stays sustained 2cm or more for several seconds–>heart cannot handle the increase in VR

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22
Q

What are signs of impaired perfusion?

A
  • Low BP (not always)

* Narrow pulse pressure (

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23
Q

Cardiac Specific signs

A
  1. Diffuse, laterally displaced PMI
    • suggests cardiomegaly and likely systolic HF
  2. Loud P2
    • pulmonary HTN
  3. RV lift
    ◦ indicative of pulmonary HTN
    • RHF in the setting of biventricular HF
  4. Tricuspid regurgitation
    • if the RV remodels in response to high afterload seen in 2nd pulmonary HTN
    • RV has impaired SV –> increased ESV and EDV
    • W/enlargement of RV, tricuspid annulus dilates
    ◦ pap muscles pulled down and apart
    ◦ leaflets can’t coapt
  5. S3, S4
    • S3 gallop during early diastole-ventricles dilated and severely compromised
    • S4 during atrial contraction- VH causing poor LV compliance (stiff)
  6. Mitral regurgitation
    - poor leaflet coapt
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24
Q

What does JVP and HJR tell us?

A

• Reflects right sided filling pressures
JVP=RAP

• Mirrors left-sided filling pressures (80%):
a) RA > 10 mm Hg, PCWP >22 mm Hg b) RA 15mmHg

• Exceptions: These may cause high JVP and HJR without increased PCWP (LAP):
-Right sided valve disease (TS, TR, PS, PR)
Pericardial disease
PHTN (pulmonary)
Isolated RV disease

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25
Q

Framingham Criteria for Dx of Congestive HF: Major criteria

A
  • Need 2 major or 1 major + 2 minor; only 70% accurate
  • Hx and PE are key!
Major: 
PND
Neck vein distension 
Rales
Cardiomegaly 
Acute Pulmomary edema (fluid in lungs) 
S3 gallop 
Increased Venous Pressure (>16 cm H20) 
Positive HJR
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26
Q

Framingham Criteria for Dx of Congestive HF: Minor

A 
Extremity edema 
Night cough 
DOE 
Hepatomegaly 
Pleural effusion (fluid around lungs) 
Vital capacity reduced by 1/3 
Tachy (120 bpm+)
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27
Q

Framingham Criteria for Dx of Congestive HF: Major or minor

A

Weight loss of 4.5+ over 5 days of treatment

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28
Q

What tests have the best sensitivity and specificity?

A
  1. HJR
  2. Orthopnea
  3. Rales is the LEAST useful finding
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29
Q

Peripheral Edema-HF or not?

A

If JVP is not elevated, the edema is not due to HF:

▫ Venous insufficiency
▫ DVT
▫ Obesity
▫ Nephrotic syndrome
▫ Cirrhosis
▫ Calcium antagonists

In addition to LE edema, be sure to look for fluid in the gut.

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30
Q

BNP

A

B-Type Naturietic Peptide

  • Produced by ventricle when diastolic pressure and wall stress are increased
  • Normal: 30-40pg.ml
  • Decompensated Heart Failure: 750 pg/ml
  • Increase Dx accuracy by 80% for patients presenting w/SOB (dyspnea)
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31
Q

Useful dx tests for HF patients: ECG

A
  • Assess cardiac rhythm and conduction
  • Detect LVH
  • Evaluate QRS duration, especially when EF is less than 35%
  • Detect evidence of myocardial ischemia
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32
Q

Useful dx tests for HF patients: CXR

A

Can see many things like:

  • cardiomegaly (very sensitive but not specific)
  • enlarged PA
  • Pleural effusion
  • Engorged veins
  • etc.

-Kerley B Lines: horizontal septal densities that extend to pleural surface = fluid in the lungs

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33
Q

BNP as Dx Tool:

A

Low levels “rule out” HF

Exceptions:

• Obesity
▫ Double BNP value of an obese patient as a correction factor

• Mitral stenosis
-LV not under stress

• Pericardial disease
-wall stress doesn’t increase

• Flash pulmonary edema
▫ Very small quantities of BNP stored in secretory granules
▫ Requirement for de novo synthesis and secretion of peptide
▫ Thus not a lot in acute setting

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34
Q

Non-HF Reasons for elevated BP

A 
• Acute pulmonary embolism
􏰂 -Associated with worse outcome (~30% pts.)
• Acute coronary syndrome 
• Pulmonary HTN
• COPD
• Pneumonia
• Renal failure
􏰂 --Impaired clearance
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35
Q

The most useful test for evaluating HF patients?

What three questions can it answer?

A

Comprehensive 2D Echo with Doppler Flow-helps determine treament

  1. Is the LV ejection fraction reduced or preserved?
  2. Is the structure of the LV normal or abnormal
  3. Are there other structural abnormalities (e.g. valvular, pericardial or RV) that could account for the clinical presentation?
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36
Q

Left-sided HF

  1. Symptoms
  2. Signs
A

Secondary to dysfunctional LV and/or left sided valvular disease

  1. Symptoms: PND, orthopnea, nocturnal cough, dyspnea, exercise limitations, fatigue, weakness, impaired mentation
  2. Signs: rales, narrow pulse pressure, pulsus alternans, cool extremities
    * NO elevated JVP!
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37
Q

Right-Sided HF

  1. Symptoms
  2. Signs
A

Most commonly due to left sided HF

  1. Symptoms: anorexia, bloating, early satiety
  2. Signs: elevated JVP, hepatomegaly, ascites, edema
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38
Q

Isolated RHF

A

• Pre-capillary pulmonary HTN

• Primary RV systolic +/- diastolic HF
▫ infiltrative disease (amyloid)
▫ RVinfarct
▫ congenital (RV dysplasia, Tetralogy of Fallot)

• Right-sided valve disease

• Pericardial disease
▫ tamponade
▫ constrictive pericarditis

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39
Q

Decompensated HF

A
  • In compensated heart failure, the dysfunctional heart is able to maintain perfusion while preserving volume status. The patient is asymptomatic or minimally symptomatic.
  • When patients decompensate, they are unable to achieve simultaneous optimized volume and perfusion. This results in symptoms or signs.

Can be harder to dx than acute HF

40
Q

Tx for Decompensated HF

A

Tx of pulmonary edema, volume overload, and/or impaired perfusion

ID and Tx underlying cause

Need good Hx and PE

41
Q

Common Factors leading to Decompensated Chronic HF

A
  1. Patient noncompliance
  2. Meds that worsen HF or renal fxn
  3. Increased fluids/salts
  4. Alcohol
  5. Arrhythmias
  6. Fever or infection
  7. MI or ischemia
  8. Worsening HTN
  9. Anemia
42
Q

Forms of HF

A
  1. Systolic or Diastolic
  2. Acute or Chronic
  3. Low output or high output
  4. Left or right-sided
  5. Forward or backward
43
Q

Systolic HF

A

Chronic systemic disorder initiated by myocardial damage:

-Impairment of pumping

  • Typically dilation of LV w/obvious impairment of contractile muscle fxn
  • reduces EF

Signs: Cold and Wet

  • Fluid overload
  • Vasoconstriction
  • Impaired Perfusion
44
Q

Diastolic dysfunction HF

A

Impairment of relaxation-prevents ventricular pressure from falling

45
Q

Acute Heart Failure

A

Serious acute injury of the heart leading to HF.
-MI, myocarditis, uncontrolled HTN

Leads to fall in CO and rapid onset of symptoms in previously normal patient

46
Q

Chronic HF

A

Chronic systolic dysfunction w/waxing and waning course of symptoms

47
Q

Acute on Chronic HF

A

When symptoms of chronic get worse

48
Q

Low output HF

A

Volume retention and progressive cardiac dysfunction from a primary abnormality in systolic function and diminished CO

49
Q

High Output HF

A

Any condition that results in chronic decrease in PVR thus causing compensatory volume retention

CO is increased, but eventually cardiac issues may develop

Causes: thyrotoxicosis, sepsis, AV shunt

50
Q

Forward failure

A

Hypoperfusion without congestion

Symptoms: impaired mentation, weakness, severe fatigue, marked exercise intolerance

Pts. often cachetic, cool extremities, narrow pulse pressure, possible pulsus alternans

Uncommon; usually only in really advanced HF

51
Q

Backward Failure

A

Symptoms due to fluid backup behind LV:

  • dyspnea
  • orthopnea
  • pulmonary edema
  • abdominal symptoms
  • LE edema

*Most common presenting symptoms of HF are backward symptoms

52
Q

Compensatory Mechanism of HF:

  1. Goals
  2. Results
A
  1. Goals of Compensatory Mechanisms:
    Maintain stroke volume, vital organ perfusion and SBP
  2. Results of Compensatory Mechanisms:
    - Vasoconstriction
    - Fluid retention
53
Q

List the 3 Compensatory Mechanisms

A

• Frank-Starling mechanism
-increased preload increases cardiac contractility

• Neurohormonal Activation

  • improve cardiac contractility
  • retain fluid and vasoconstrict nonessential vascular beds to maintain perfusion to vital organs

• Myocardial and Vascular Remodeling
-increase mass of cardiac tissue and raise arterial resistance

54
Q

Most common presentation of symptomatic HF

A

-Excess fluid volume with compensatory vasoconstriction combined with LV dysfunction

55
Q

Three Mechanisms to increase CO:

A
  1. Increase heart rate
  2. Increase preload
    - increase in VR causes mild dilation of ventricle
  3. Increase contractile state
    - hop to new FS curve
56
Q

Frank Starling Mechanism

A
  • Increases contractility (SNS activation) and preload
  • In normal hearts, increased preload stretches myocytes, increases overlap between actin and myosin, and increases contractile force
57
Q

Normal Exercise Response

A

• Increased sympathetic nervous system activation: β1 binding

▫ Increased depolarization of automatic SA node cells: increase HR

▫ Increased preload
-catecholamines cause venoconstriction leading to increased VR

▫ Increased calcium influx, increased force of contraction

58
Q

Exercise Response in HF

A 
• Depressed contractility at baseline
• Chronic sympathetic nervous system
activation leads to...
• Decreased adrenergic responsiveness:
􏰂 -Down-regulation of β1 receptors
􏰂 -Uncoupling of receptors from intracellular messenger systems

THUS:
• Inability to increase contractility normally
• thus, HF pts increase SV primarily through increased preload (right shift)

◦ As long as PCWP doesn’t get too high from increasing preload then no problem

◦ if PCWP too high–>
Pulmonary Congestion
(push fluid into alveolar space)–>
dyspnea

59
Q

What neurohormones are high in HF?

A

Excess vasoconstriction!

Constrictors:

Endothelin 
Aldosterone 
Angiotensin II 
Vasopressin 
Norepinephrine

Dilators:
NO
ANP
Increased BNP

  • Goal of both of these is to redistribute CO.
  • Tx targeted to balance these 2
60
Q

RAAS

A
  • Renin-angiotensin-aldosterone system is highly activated in HF
  • Renin is released in response to low renal perfusion pressure, decreased filtered sodium and SNS activation
  • Renin cleaves angiotensinogen to AT-I
  • ACE: AT-I􏰄 to AT-II
  • AT-II stimulates aldosterone release (fluid and salt retention)
61
Q
  1. Cardiac Effects of Angiotensin II

2. Vascular Effects

A
  1. Cardiac:
    a) Increases contractility (modest)

􏰂 b) Increases afterload (good at first to perfuse brain, bad later)
-it’s a vasoconstrictor

􏰂 c) Indirectly increases preload
• by increasing Na+ and H20 retention

􏰂d) Cardiac remodeling

  • myocyte hypertrophy
  • possible increase in mitosis without angiogenesis which promotes fibrosis
  1. Vascular effects: 􏰂 Vasoconstriction
62
Q

RAAS

  1. Renal Effects
  2. Other Ex
A
  1. Renal Effects:
    a) Efferent > > afferent arteriolar constriction
    - Increases filtration fraction of the RBF

*􏰂b) Increased sodium absorption in proximal tubule

􏰂*c) Increased sympathetic nervous system activation

􏰂*d) Distal tubule Na + absorption via aldosterone
􏰂 􏰅
e) Increase Mesangial contraction decreasing􏰆 glomerular surface area

  1. Other Effects
    Stimulates Thirst
63
Q

RAAS:

  1. Acute Compensatory Effects:
  2. Long-term Detrimental Effects:
A
  1. Acute compensation:
    􏰂 Vasoconstrictor effects dominate – arterial pressure is maintained
  2. • Long-term detrimental effects:
    􏰂-Cardiac fibrosis and hypertrophy with subsequent ventricular remodeling

􏰂-Possible mismatch of ventricular muscle mass and capillary density

-Vasoconstriction􏰇􏰅 increases afterload􏰇 causing ventricular remodeling

  • Salt and water retention
    • remember that fluid overload is responsible for most of the symptoms!
64
Q

ACE-Inhibitors and HF

A

Target RAAS:

• ACE inhibitors were the first neurohormonal blocking drugs shown to benefit patients with heart failure

• ACE Inhibitors
-􏰂 Reduce HF mortality by 20-30%
􏰂-Reduce cardiac related hospitalizations
􏰂-Improve exercise capacity
􏰂-Retard the progression of LV remodeling

65
Q

SNS in HF

A
  1. SNS highly activated in heart failure
    • Normally, baroreceptors are active and inhibit sympathetic; they keep BP down/normal
    • BUT in HF, baroreceptors sense low SV so they are inhibited
  2. Parasympathetic traffic decreased
  3. Baroreceptor and mechanoreceptor-
    mediated tonic inhibition of the SNS decreases

• Muscle metaboreceptor excitatory input increases

66
Q

Cardiac Effects of NE

A

Cardiac effects of norepinephrine:

The Good:
􏰅 -increases Heart rate
􏰅 -increases Contractile force (positive inotropy)
􏰅 -increases Speed of relaxation (positive lusitropy)

The Bad:
􏰅-increases Ventricular arrhythmias
-Myocyte toxicity secondary to calcium overload can lead to Myocyte death

*Blocking NE effects with BB decreases mortality

67
Q

NE Vascular Effects:

A
  • Vasoconstrictor in splanchnic beds

􏰂-Vasodilator in skeletal beds

**- Activation of renin-angiotensin system 􏰃leads to vasoconstriction
􏰂
**-Net effect is arterial vasoconstriction
􏰂
-Venoconstrictor
• can increase VR to the heart

68
Q

NE Renal Effects

A

􏰂-Renal vasoconstrictor

􏰂-Direct effect to increase sodium absorption in the proximal convoluted tubule

􏰂 -Renal sodium and water retention 􏰂 􏰅

-Increase Renin release

69
Q

SNS: NE

  1. Acute Compensation
  2. Long-term detrimental effects
A

• Acute compensation:
􏰂 􏰅 -increase cardiac output via 􏰅 increase heart rate and 􏰅
contractility
􏰂 -Redistribution of blood to vital organs

• Long-term detrimental effects:
􏰂 􏰅- increase ventricular arrhythmia
􏰂 -vasoconstriction 􏰇 􏰅 leading to increased afterload 􏰇–> ventricular remodeling
􏰂 -myocyte damage and death
􏰂 -salt and water retention (direct & via RAAS)

70
Q

SNS Therapy

A

• Beta blockers are standard therapy in CHRONIC systolic HF
• Reduce mortality by~35%
• Reverse remodeling
– takes weeks to months
• Paradoxic improvement in systolic function
• Not all BBs equal

DO NOT USE AS RESCUE THERAPY IN ADHF OR CARDIOGENIC SHOCK!!

71
Q

Aldosterone:

  1. Cardiac Ex
  2. Vascular
  3. Renal
A
  • Cardiac effects of aldosterone: 􏰂 cardiac fibrosis
  • Vascular effects: 􏰂 vascular fibrosis

• Renal effects:
􏰂 sodium absorption in the distal tubule

72
Q

Aldosterone:

  1. Acute comp.
  2. Long-term detrimental Ex
A

• Acute compensation:
􏰂 Increase plasma volume to maintain blood pressure

• Long-term detrimental effects:

􏰂 -Increased cardiac stiffness, worsened diastolic and systolic function, adverse remodeling

􏰂- Increased vascular stiffness, increased afterload

􏰂-Sodium & volume retention

  • Potassium, magnesium loss
73
Q

Aldosterone System Tx

A
  • Aldosterone blockade has been shown to reduce death in patients with moderate-to- severe heart failure and in those with post MI systolic dysfunction
  • Hyperkalemia is a significant side effect

MRA drugs: spironolactone, eplerenone, new agents

74
Q

Natriuretic Peptides

A

• Small peptides secreted by the heart muscle in response to increased chamber pressure and wall stress
• ANP,BNP
• Vasodilators, mild diuretic properties
• Levels of ANP&BNP are elevated in HF
• Degree of elevation correlates with severity of disease
We DO measure BNP routinely

75
Q
  1. Cardiac effects of natriuretic
    peptides:
  2. Vascular
  3. Renal
A
  1. 􏰂 None known
  2. Vascular effects:
    -􏰂 vasodilation
    􏰂 􏰆- decreased vascular fibrosis and hypertrophy 􏰂 􏰆
    -decreased vascular stiffness
  3. Renal effects:
    􏰂 􏰆 -decreases sodium absorption in the proximal tubule–> natriuresis
    -Water follows the sodium, resulting in a mild diuresis
76
Q

Natriuretic Tx

A

Intravenous human recombinant BNP can be given to increase vasodilation and relieve symptoms in decompensated HF patients.

77
Q

NO

A
  • Role of NO in HF unclear
  • Data suggest the NO heart has negative inotropic effects (not necessarily bad as the beta blocker story tells us….)
  • May mediate oxidative damage and apoptosis in the heart
  • May also have beneficial cardiac effects due to localization
  • Clear relative deficiency of vascular NO in heart failure
  • NO is a vasodilator
  • Possibly very important in African Americans w/HF
  • Way less NO in HF
78
Q

Deleterious Effects of Inflammatory Mediators in HF

A
  • Left ventricular dysfunction
  • Pulmonary edema
  • Cardiomyopathy
  • Reduced skeletal muscle blood flow
  • Endothelial dysfunction
  • Anorexia and cachexia
  • Receptor uncoupling
  • Activation of the fetal gene program
  • Cardiac myocyte apoptosis
79
Q

Inflammation Tx

A

Not helpful!

TNF alpha blocker drugs make HF worse

80
Q

Concentric Remodeling

A

1) In a NORMAL myocardium, the response to PRESSURE overload includes:
􏰂 -Parallel addition of sarcomeres
􏰂 -Wall thickening

= Concentric hypertrophy

-􏰂 Compensatory and may allow for stable function for many years
􏰂-Neutralizes wall stress

81
Q

Eccentric Remodeling

A

1) In a NORMAL myocardium, the response to VOLUME overload includes:
􏰂 -Addition of sarcomeres and myofibrils in series
􏰂 -Chamber enlargement

= Eccentric hypertrophy

􏰂 -Compensatory and may allow for stable function for many years
-Increase in wall stress
• can beget further remodeling

***can contribute to the preservation of stroke volume despite reduced LVEF


82
Q

Post-MI Remodeling

A

1) Post-infarct, necrotic area expands (hours)

2) Infarct expansion (hours to days)
- hypercontractile adjacent myocardium
- ->increased wall stress
- ->increased extracellular matrix deposition
* ACE-I’s and BBs can be effective in reverse remodeling

3) Eccentric global remodeling
- redistribution of uneven wall stress
- SPHERICAL
- greater likelihood of morbidity and death

83
Q

HF Remodeling

A
  • Pressure AND volume overload occur due to vasoconstriction and volume retention
  • Eccentric remodeling predominates
  • The ventricle is more spherical
  • Relentless injury to the myocardium due to underlying disease process and neurohormone mediated damage
  • Secondary AV valve regurgitation due to dilation of AV annulus
84
Q

Molecular Changes in Remodeling of the Heart in HF:

Fetal Gene

A

1) Switch to “fetal” gene program
􏰂 -α-myosin –> β-myosin (not as good contractility)
􏰂 -Altered cytoskeletal proteins

• Occurs 2° to mechanical stress, neurohormones, inflammatory cytokines, reactive oxygen species

85
Q

Molecular Changes in Remodeling of the Heart in HF:

SERCA

A
  1. DECREASE SERCA expression
    (Sarcoplasmic ER Ca2+ ATPase)
    -normally does reuptake of Ca2+ into SR during diastole

􏰂-Ryanodine receptor leak

  • Decreased systolic calcium levels
  • increased diastolic calcium levels
86
Q

Molecular Changes in Remodeling of the Heart in HF: List

A
  1. Switch to fetal contractile gene program
  2. altered Ca2+ handling/transient, electrical remodeling
    - Slowed kinetics, prolongation
    - SERCA decrease
  3. Changes in metabolic enzyme profile
  4. Changes in collagen isoform and ECM composition
  5. Myocyte Injury and loss
87
Q

Ventricular Remodeling

  • Prognosis
  • Tx
A

• Remodeling shown to be associated with worse prognosis

• Many neurohormonal therapies (ACE inhibitors, beta blockers, aldosterone antagonists):
-reverse the remodeling process, both at the anatomic level and the molecular level

􏰂* Beta blocker “responsive” patients increase levels of α-myosin heavy chain

88
Q

General Tx plan for Decompensated HF?

A

• Remember, this patient is fluid
overloaded and….vasoconstricted

• The solution is to help the heart move the fluid forward out of the venous system into the arteries……. 􏰇 VASODILATION.

89
Q

Stages of Heart Failure: A

A

High risk for developing HF, but no structural heart disease of symptoms of HF

90
Q

Stages of Heart Failure: B

A

Structural HD but no signs/symptoms of HF

91
Q

Stages of Heart Failure: C

A

Structural HD with prior or current signs/symptoms of HF

92
Q

Stages of Heart Failure: D

A

Refractory HF requiring special interventions

93
Q

General guidelines for chronic HF management

A
  1. Once Stage B (structural HD)-give ACE-Is and BBs even w/out symptoms
    - decrease remodeling
  2. ACE-I
    - improves life quality
    - increases exercise capability
    - reduces HF hospitalizations and mortality
    - These effects secondary to hemodynamic unloading of the heart (vasodilation) and anti-fibrotic, anti-remodeling effects
  3. Chronic BB–promotes reverse remodeling
    - decreases LV sphericity
    - reduces V diameter
    - increased contractility
    - dramatic reduction in HFrEF hospitalizations and mortality
  4. MRA therapy (aldosterone blocker)
    - add to pts who continue to have severe sx even w/ACE-Is and BBs
    - improve survival
94
Q

Positive Inotropic drugs and HF

A

Surprisingly not helpful at all

  • ->fatal V. arrhythmias
  • ->possibly b/c some are vasoconstrictors and a lot of these patients have CAD

**Dobutamine and milrinone somewhat helpful b/c vasodilatory and increase contractility

*Reserved for stage D, palliative care, or awaiting transplant

95
Q

General drug schedule for HF

A

diuretics, vasodilators, neurohormonal blocking agents (ACE-Is, ARBs, BBs)

CV (11 decks)

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