CHF 1 Flashcards

1
Q

What increases your risk of Heart failure?

A
increase with age
coronary heart disease
cigarette smoking
HTN
Obesity
Diabetes
Valvular heart disease
Race African Amer.> Caucasian
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2
Q

What is the most common causes of heart failure according to an italian registry of 6,200 patients?

A

Ischemic heart disease 40%
Dilated cardiomyopathy 32%
Primary Valvular Dz-12%
HTN-11%

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3
Q

what is the most common causes of heart failure in developing countries?

A

HTN-33%
Idiopathic Cardiomypoathy-28%
Ischemic Heart Dz-9%
Rheumatic Fever 8%

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4
Q

In In 2007 the AHA estimated how many people in the US and world wide have heart failure

A

5.7 million people in the US and 23 million world wide have heart failure.

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5
Q

What happens with calcium during Heart failure?

A

Calcium influx results in decreased efflux from the SR, resulting in decreased contractile strength and poor relaxation
Note: low pH decreases the ability for calcium to bind to troponin C resulting in decreased contractions

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6
Q

what determines stroke volume?

A

preload, contractility and after load

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7
Q

What does end diastolic volume (preload) vs SV(CO+HR) tell us

A

it tells us that if you improve the preload then you will improve the stroke volume to a point. This helps to determine fluid resuscitation

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8
Q

What happens to afterload in heart failure

A

these changes are enhanced where the resistance that ventricle meets during systole increase

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9
Q

Describe how contractility, afterload and preload can exacerbate or ameliorate symptoms.

A

When these are not function correctly fluid gets backed up into the Lymphatics and into the lungs. It makes blood vessels plumper and will thicken interstitial space and make lungs thicker. You will see pleural effusion because it can not handle the volume

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10
Q

what is heart failure

A

Clinical syndrome of the inability of the heart to keep up with the demands on it and, specifically, failure of the heart to pump blood with normal efficiency

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11
Q

what are the two types of heart failure

A

Two types of HF that can effect both the left side and the right side
Systolic- it cant squeeze it forward
Diastolic- can fill it

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12
Q

what is systolic dysfunction?

A

Decreased myocardial contractility.

Think of the spring where the coils are too far pulled apart and they lost there “springiness.”

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13
Q

What is the result in systolic dysfunction when there is decreased myocardial contractility?

A

results in decreased SV which results in decreased CO.

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14
Q

What is the bodies response to systolic dysfunction?

A

Neurohormone response to increase contractility and HR to maintain homeostasis. (work to keep alive but your limping on, the backup systems are just ok at functioning)
Angiotensin, Cathecholimines, antidiuretics pathways to regulate BP
Kidneys hold onto sodium resulting on water retention and volume expansion to maintain preload
Calcium looses its affinity of troponin C in vitro possibly from muscle stretch at the sarcomere level.
Cardiac myocyte is nml diameter and increased in length. (no change in LV wall thickness and increased in LV volume)

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15
Q

what is dyastolic dysfunction?

A

Diastolic Heart Failure is when the pt has clinical signs of heart failure in the setting of normal ejection fraction.

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16
Q

what happens with diastolic dysfunction in term of their Stroke volume?

A

SV is preserved but an increase in end diastolic pressure, resulting from decreased compliance to receive a certain amount of volume.
Generally a concentric pattern of LV remolding and a hypertrophic process characterized by
A normal or near nml EDV
Increased Wall Thickness
An increased ratio of myocardial mass to cavity volume
An increased ratio of wall thickness to chamber radius

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17
Q

What is the role of neurohumoral response?

A

Body compensates for decreased CO in order to maintain homeostasis by:
Maintain systemic vasoconstriction
Increase contractility and HR by improving volume expansion.

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18
Q

what are the 6 types of neurohumoral responses by the body for decreased CO

A
RAAS
ADH (volume expansion)
ANP (vasodilator)
Nitric oxide (vasodilator)
Endothelin (vasoconstrictor)
Sympathetic nervous system (improves contractility, vasoconstrictive, and HR)
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19
Q

What are complications of neurohumoral response?

A
  • Elevated Diastolic pressure to the atria and pulmonary/systemic venous circulations resulting in pulmonary congestion and edema
  • Increased afterload in an attempt to vasocontsrict the peripheral systemic system.
  • Catecholamines used to increase contractility and HR increase risk for coronary ischemia.
  • Catecholamines and Angiotensin II promote apoptosis of myocytes.
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20
Q

What are symptoms of right sided heart failure?

A
DOE
Fatigue
Syncope
Exertional angina
Anorexia
Hepatomegaly
JVD
Split S2
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21
Q

What is the Tx for Right sided HF

A
Treat the underlying cause
Pulmonary HTN
PE
COPD
OSA
L sided failure
No Digoxin as it has no evidence that it helps and may have deleterious effects
If in cardiogenic shock attempt IV inotropic agents (dobutamine and milrione)
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22
Q

what are the 5 classes of cardiomyopathy?

A
Dilated
Hypertrophic
Restrictive
Arrhythmogenic Right Ventricular
Unclassified
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23
Q

Cardiomyopathy is based on specific cardiac disorders or systemic disorders such as?

A
Ischemic
Valvular
HTN
Inflammatory
Metabolic
Toxic
Genetic
Two types
Primary
-Genetic or acquired
Secondary
-When other organ systems are involved
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24
Q

what is dilated cardiomyopathy?

A

Dilation and decreased contractility of one or both ventricles (i.e. decreased systolic function)
Associated with Hypertrophy in severe disease

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25
Q

how will a dilated cardiomyopathy show up on echo?

A

Echo shows dilated LV, becomes more round than the nml ovoid, nml or decreased wall thickness, poor wall thickening and/or reduced inward endocardial systolic motion. LA enlargement, RV enlargement and dysfunction

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26
Q

what are the causes of dilated cardiomyopathy?

A
Idiopathic 50%
Myocarditis 9%
Ischemic 7%
Infiltrative 5%
Peripartum 4%
HTN 4%
HIV 4%
Connective Tissue Disease 3%
Substance Abuse 3%
Doxorubicin 1% (shows up on boards)
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27
Q

what is hypertrophic cardiomyopathy?

A

Hypertrophied LV, and occasionally the RV
Usually the intraventricular septum compared to the LV free wall
Concentric hypertrophy involves both
Apical Hypertrophy
LV volume is nml or reduced and associated with with diastolic dysfunction
Increased risk of sudden cardiac death(specifically when it’s the left ventriclular wall septum
Characterized by a mid systolic harsh murmur that worsens with valvsalva (bearing down)

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28
Q

What is the cause of hypertrophic cardiomyopathy?

A

Hypertrophic
60-70% is genetic mutation of sarcomere proteins
Autosomonal dominant
Check routine ECHOs in 1st degree relatives
Acquired causes
HTN and Aortic stenosis
Heart needs to push against a high pressure
Arrhythmias are common

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29
Q

how is hypertrophic cardiomyopathy treated?

A

Avoid stress activities
TX Beta blockers (1st line) dihydro CCB (2nd line)
Diuretics, ICD, rate control, surgery, ETOH septal ablaation

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30
Q

what is restrictive cardiomyopathy?

A

Non-dilated, non-hypertrophied ventricles with impaired filling. Biatrial enlargement (secondary to elevated pressures)
Systolic function is nml in the early stages
RV failure more common than LV

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31
Q

how are restrictive cardiomyopathies classified?

A

Infiltrative (amyloid (most common), sarcoid, hematochromotosis)
Noninfiltrative (scleroderma, idiopathic, genetic)
Storage Diseases (hematochromotosis, Fabry Disease (alpha glaactosidase A))
Endomyocardial Diseases (endomyocardial fibrosis, hypereosinophillic syndrome, anthracycline fibrosis, radiation)

32
Q

what are the treatments for restrictive cardiomyopathies?

A
  • Amyloid Tx is transplant vs chemo vs stem cell transplant
  • Sarcoid Tx is steriods, chloroquine, cyclosporine, methotrexate
  • Hematochromotosis Tx is phelbotomy and iron chelation ? Heart transplant
  • Endomycoardial diesase tx is warfarin
  • Hypereosinophillia tx is steriods, interferion, cyclosporine and warfarin
  • Fabry’s tx is alpha galactosidase A replacement
33
Q

what is arrythmogenic right ventricular?

A

Genetic disease with ventricular arrhythmias and RV free wall fibrosis and/or fibro-fatty tissue with scattered residual myocardial cells.
Regional or global akinesis or dyskinesis of the RV

34
Q

what is athletes heart?

A

Intensive endurance training results in increase in LV wall thickness, cavity size, and mass
Associated with benign arrhythmias but some can be lethal
Need to rule out other underlying causes of hypertrophy, LVH is generally symmetric and ≤ 12 mm

35
Q

what are types of unclassified cardiomyopathies?

A

Endocardial Fibroelastosis
Fibrosis and elastic tissue involvement of the LV
Occurs in infants within the first two years of life
Left Ventricular Noncompaction
Rare

36
Q

What is takotsubo cardiomyopathy?

A
(stress-induced)
“Broken Heart Syndrome”
 Apical ballooning of the LV in systole
 More common in women
Clinically can present as an MI
Uncertain etiology
Catecholamine surge, coronary artery spasm, mirovascular dysfunction
Mortality of 0-8 %, typically recover function within 1-4 wks
37
Q

what are the 4 criteria needed to classify something as peripartum cardiomyopathy?

A

4 criteria needed

  • Development of cardiac failure in last month of pregnancy or within 5 months of delivery
  • Absence of an identifiable cause of HF
  • Absence of recognizable heart disease prior to last month of pregnancy
  • LV systolic dysfunction
38
Q

what are the risk factors for peripartum cardiomyopathy?

A

> 30 yo, Multiparity, African descent, multiple fetuses, Hx pre-/eclampsia, postpartum HTN, maternal cocaine abuse, > 4 wks use of tocolytic (to prevent contraction) use.

39
Q

Alcoholic cardiomyopathy

A
  • Large amounts of alcohol is associated with cardiomyopathy
  • Pronounced LV dilation, increased LV mass, thin/nml LV walls, diastolic dysfunction (asymptomatic) and systolic dysfunction (symptomatic)
  • Uncertain etiology
  • ETOH induces apoptosis
  • Acute and transient toxic effect on cardiac performance
  • Nutritional Deficiency, esp thiamine(B1) which can lead to Beriberi
  • Additives in alcoholic beverages, i.e. cobalt, can rarely have toxic effects on the heart
  • Need to stop drinking
40
Q

mitral stenosis causes

A

Often the result of rheumatic fever(caused by strep)
Other causes are:
Calcification of the valve
Abnormal papillary muscles

41
Q

what happens with mitral valve stenosis?

A
  • Decreased flow out of the atria results in high atrial pressures resulting in back flow into the pulmonary vasculature.
  • Usually a gradual progression of increased pressures and in mild-moderate disease the lymphatic system can drain the extra fluid.
  • In the setting of increase HR and decreased diastolic filling time fluid backs up more and the lymph system cannot drain that extra fluid
42
Q

characteristics of mitral stenosis on exam

A

Opening snap following S2

Diastolic murmur loudest in mitral area

43
Q

Mitral valve stenosis treatment?

A
-Rate control heat rate
Warfarin if in afib
-Surgery (in severe disease)
Percutanteous valvuloplasty
Open replacement (usually if there is both stenosis and regurg)
44
Q

what is mitral regurgitation?

A

Fluid is shot back up into the LA during systole due to an incompetent valve. This results in an enlarged LA
-Characterized by
Pansystolic murmur at the apex radiating to the axilla
Systolic murmur heard over the mitral area

45
Q

what causes mitral valve reguritation?

A

Papillary muscle failure/dysfunction
Enlarged mitral annulus
Dilated cardiomyopathies
Ischemic heart disease

46
Q

what is a result of mitral valve regurgitation?

A

Can cause LV failure due to a decreased CO leaving the heart into the aorta.

47
Q

mitral valve Tx

A

Asymptomatic failure has no treatment
Most symptomatic failure requires symptom management
Decreased CO from MR may result in the need for valve repair.

48
Q

what is the most common cause of acute mitral regurg

A

Chordal rupture

49
Q

what are other causes of mitral regurg

A

Also by MI, Endocarditis, Prosthetic Valve Dysfunction.

50
Q

what is a result with mitral regurg

A

LA is not compliant and does not tolerate regurgitant flow well resulting in increased flow into the pulmonary circulation

51
Q

what is mitral valve prolapse and who is it most common in?

A

Floppy” Valve

Most are female

52
Q

what causes mitral valve prolapse?

A
Hyperadrenergic state
Connective tissue diseases
Ehlers-Danlos
Marfan
Chordae rupture
53
Q

How is mitral valve prolapse characterized?

A

mid systolic clicks

54
Q

how do you treat mitral valve prolapse?

A

Beta blockers for hyperadrenergic state

surgical repair

55
Q

what are causes of aortic stenosis?

A
-Congenital
Uni-cuspid valve
Bi-cuspid valve
-Degenerative or calcific
25% over age 65 and 35% over age 70
56
Q

aortic stenosis is characterized by?

A

systolic murmur in aortic area

57
Q

what are symptoms of aortic stenosis?

A

Angina (decrease flow to endocardium)
Syncope
Hypotension

58
Q

what is the tx for aortic stenosis?

A

surgery

59
Q

left ventricular outflow tract obstruction is causes by

A
Caused by 
Aortic Stenosis  
Supravalvular Stenosis
Subvalvular Stenosis
Hypertrophic Cardiomyopathy
Genetic Disorder
Severe Systemic HTN
60
Q

what is the number one cause of aortic regurgitation?

A

rheumatic heart disease

now its congenital (bicuspid valve), endocarditits, HTN, marfans, aortic dissection

61
Q

what are characteristic of aortic regurgitation?

A

diastolic murmur over aortic area

most patients are asymptotic

62
Q

how do you treat aortic regurgitation?

A
Treatment is usually the underlying disease
Severe AR (or infectious endocarditits) may need surgical repair
Decreased afterload will help reduce amount of blood back into the LV
63
Q

what is acute aortic regurgitation?

A

The LV cannot compensate for the rapid filling during diastole which is caused by regurgitant blood.

64
Q

right sided valve disease notes

A
  • Same things that happen on the Left can happen on the Right.
  • However due to the lower pressures the severity of the disease is not as evident
65
Q

tricuspid stenosis is causes by?

A

Usually as a result of valve repair, replacement or to carcinoid.
Not very common now that rheumatic heart dz is rare

66
Q

what type of murmur would you hear with tricuspid stenosis

A

Diastolic “rumble” that worsens with inspiration

67
Q

how to treat tricuspid stenosis

A

reduce fluid congestion

valve replacement

68
Q

tricuspid regurgitation

A
  • Very common
  • Usually asymptomatic
  • Common in pts with pulmonary disease
  • Treat with diuretics for fluid congestion
  • If surgical repair planned for mitral valve will repair tricuspid at same time
69
Q

pulmonic regurgitation

A

Usually from pulmonary hypertension
Can be due to dilated annulus
Symptom management

70
Q

acute heart failure physiology

A
  • Heart failure either acute on chronic or new onset resulting in pulmonary capillary congestion causing shortness of breath and possibly respiratory failure.
  • Decreased CO results in rapidly increasing LV filling pressures, LA pressure and filling of the pulmonary capillary bed.
  • The increase in fluid overwhelms the lymphatic drainage system
71
Q

what does stage 1 of congestive heart failure look like on a CXR

A

redistribution of pulmonary vessels

Cardiomegaly

72
Q

what does stage 2 of congestive heart failure look like on a CXR

A

Kerley lines
Peribronchial cuffing
thickened interlobar fissures

73
Q

what does stage 3 of congestive heart failure look like on a CXR

A

consolidation
air bronchogram
cottolwool appearance
plueral effusion

74
Q

what are the 2 ways to classify causes of acute heart failure?

A
  • chronic cardiac conditions that predispose decompensation

- triggers that precipitate decompensation

75
Q

what are Chronic cardiac conditions that predispose decompensation.

A

Systolic Dysfunction
Diastolic Dysfunction
Left Ventricular Outflow Tract Obstruction
Mitral Stenosis

76
Q

what are Triggers that precipitate decompensation

A
Myocardial ischemia/infection
Acute Aortic Regurgitation
Acute Mitral Regurgitation
Reno-vascular HTN
LA outflow impairment
Volume Overload
77
Q

ischemic heart disease

A
  • HF can occur in the setting of CAD without acute coronary syndrome.
  • Decreased flow to the myocardium can result in systolic and/or diastolic HF
  • Can cause/worsen valvular disease