Congestive Heart Failure Part 1 Flashcards

1
Q

Epidemiology of Heart Failure

A

In 2007 the AHA estimated 5.7 million people in the US and 23 million world wide have heart failure.

Risk increases with age, coronary heart disease, cigarette smoking, HTN, Obesity, Diabetes, Valvular Heart Disease, Race (68% vs 49% in African Americans compared to Caucasians)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Causes of Heart Failure (4)

A
Ischemic Heart Disease 40%
Dilated Cardiomyopathy 32%
Primary Valvular Disease 12 %
Hypertensive Heart Disease 11%
Other 5%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Developing Countries causes of HF (6)

A
Rheumatic Fever
Valvular 8%
Peripartum Cardiomyopathy
Idiopathic Cardiomyopathy 28%
Hypertension 33%
Ischemic Heart Disease 9%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Action Potential

A

The creation of the the action potential in one area results in the creation of another action potential in the adjacent area, and repeats.
Linear propagation occurs because the myocytes along muscle fibers are electrically continuous.
For the above two reasons the action potential results in a “wave.”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Muscle Contraction

A

Tropomyosin physically blocks the interaction between the thick and thin filaments
Three types on troponin I, T and C
C binds calcium which allows the thick and thin filaments to interact.
I inhibits the ATPase of actomycin and helps calcium bind to C
T attaches the troponin complex to actin and tropomyosin, blocks the actin-myosin binding site at rest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Calcium in HF

A

Ca is found in the sarcoplasmic reticulum
Low pH decreases the ability for calcium to bind to troponin C resulting in decreased contractions.
Heart failure
Calcium influx results in decreased efflux from the SR, resulting in decreased contractile strength and poor relaxation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Normal Left Ventricular Pressure-Volume Relationship

A

When thinking about this, think of a spring.
Volume enters the LV and at the end of diastole the LV fibers are stretched.
This Stretch is determined by the resting force, myocardial compliance, and how much filling from the L atria. This distension force is PRELOAD.
CONTRACTILITY is the force generated by the myocardium
AFTERLOAD the resistance the LV works against during systole.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Frank Starling relationship

A

EDV (preload) vs SV (CO + HR)

Improve the preload and the SV will improve (to a point)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Afterload

A

The resistance that ventricle meets during systole.
In a nml heart the SV changes minimally to changes in afterload.
In the failing heart these changes are enhanced.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Contractility

A

The ability for each myocyte to contract ( a function of calcium)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Definition of 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Two types of HF that can effect both the left side and the right side

A

Systolic

Diastolic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Systolic Dysfunction (2)

A

Decreased myocardial contractility.

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Issues with Systolic Dysfunction (5)

A

Decreased contractility results in decreased SV which results in decreased CO.
Neurohormone response to increase contractility and HR to maintain homeostasis.
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Diastolic Dysfunction

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Problems with Diastolic Dysfunction (7)

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

Cardiac myocyte is thickened with no change in length. (change in LV wall thickness and no change in LV volume)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Neurohumoral Response (3)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Different Pathways of Neurohumoral Response

A

Renin-angiotensin-aldosterone system
Angiotensin II increases sodium reabsorption and causes systemic and renal vasoconstriction and can cause pathological remodeling
Antidiuretic hormone (volume expansion)
Atrial Natriuretic Peptide (vasodilator)
Nitric oxide (vasodilator)
Endothelin (vasoconstrictor)
Sympathetic nervous system
Catecholamines
Norepinephrine (improve contractility, vasoconstriction and HR)
Can lead to myocyte pathological remodeling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Complications of Neurohumoral Response (4)

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Right Sided Heart Failure

A

Known as Cor Pulmonale when cause by pulmonary HTN that is associated with lung disease, primary pulmonary HTN, OSA, or chest wall abnormalities (kyphoscoliosis)
L side failure can “spill over” into the R sided but it is NOT called Cor Pulmonale.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Manifestations of Right Sided Heart Failure (8)

A
Slow and progressive unless PE
DOE
Fatigue
Syncope
Exertional angina
Anorexia
Hepatomegaly
JVD
Split S2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Right Sided Failure Treatment (7)

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Cardiomyopathy

A

are heterogeneous group of diseases of the myocardium associated with mechanical and/or electrical dysfunction that usually (but not invariably) exhibit inappropriate ventricular hypertrophy or dilatation and are due to a variety of causes that frequently are genetic, either are confined to the heart or are a part of generalized systemic disorders, often leading to cardiovascular death or progressive heart failure related disability.”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

5 classes based on anatomy and physiology for Cardiomyopathy

A
Dilated
Hypertrophic
Restrictive
Arrhythmogenic Right Ventricular
Unclassified
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

2 Types of Cardiomyopathy

A

Primary
Genetic or acquired
Secondary
When other organ systems are involved

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Based on specific cardiac or systemic disorders for Cardiomyopathy (7)

A
Ischemic
Valvular
HTN
Inflammatory
Metabolic
Toxic
Genetic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Dilated–Cardiomyopathy

A

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

28
Q

Causes of Dilated Cardiomyopathy (10)

A
Idiopathic 50%
Myocarditis 9%
Ischemic 7%
Infiltrative 5%
Peripartum 4%
HTN 4%
HIV 4%
Connective Tissue Disease 3%
Substance Abuse 3%
Doxorubicin 1%
Other 10%
29
Q

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
Characterized by a mid systolic harsh murmur that worsens with valvsalva

30
Q

Hypertrophic Cardiomyopathy Epidemiology and Etiology

A

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

31
Q

Restrictive Cardiomyopathy (3)

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

32
Q

Restrictive Cardiomyopathy Classified as:

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)

33
Q

Arrhythmogenic Right Ventricular Cardiomyopathy

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

“Athlete’s Heart”
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

34
Q

Unclassified Cardiomyopathy (4)

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

35
Q

Takotsubo (stress-induced) Cardiomyopathy

A
“Broken Heart Syndrome”
Takotsubo is Japanese for Octopus trap
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
36
Q

Peripartum Cardiomyopathy (4)

A

Rare cause
Cause is unknown
Cytokine release, Myocarditis, Abnormal immune response, Genetic, Hemodynamic changes

37
Q

Peripartum Cardiomyopathy 4 Criteria

A

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

Risk Factors and Prognosis of Peripartum Cardiomyopathy

A

Risk Factors
> 30 yo, Multiparity, African descent, multiple fetuses, Hx pre-/eclampsia, postpartum HTN, maternal cocaine abuse, > 4 wks use of tocolytic use.

Prognosis
Cardiac Transplant 4-7%
Mortality 6-23%
Recovery of function (EF > 50%) 54%, better in pts with a baseline EF > 30%
Pacer placement 2-3%
Mean EF recovery increased from 28 to 46%

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 which can lead to Beriberi
Additives in alcoholic beverages, i.e. cobalt, can rarely have toxic effects on the heart
Need to stop drinking
Prognosis is similar to or slightly worse than idiopathic cardiomyopathy

40
Q

Infectious Cardiomyopathy (8)

A
Viral
Coxsackie
Influenza
Adenovirus
Echovirus
CMV
HIV
Chagas Disease
Lyme Disease
41
Q

Toxic Cardiomyopathy (4)

A

EOTH
Cocaine
Chemotherapy drugs (anthracycline)
Trace elements overloads (mercury, gold, antimony, chromium, cobalt, arsenic) deficiencies (selenium)

42
Q

Valve

A

a membranous fold in a hollow organ or tubular structure, such as a blood vessel or the digestive tract, that maintains the flow of the contents in one direction by closing in response to any pressure from reverse flow.

43
Q

Function of Valve

A

1) NOT allow flow through (or at least limit it), medically called stenosis
2) Allow flow BACK through, medically called regurgitation

44
Q

Mitral Stenosis Causes

A

Often the result of rheumatic fever
Other causes are:
Calcification of the valve
Abnormal papillary muscles

45
Q

Mitral 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

46
Q

2 Characteristic Findings on the Exam for Mitral Stenosis

A

Opening snap following S2

Diastolic murmur loudest in mitral area

47
Q

Mild- Severe Mitral Stenosis

A

Mild to moderate stenosis
Usually asymptomatic can be slightly symptomatic

Severe stenosis
Awful disease
Pulm HTN, RV failure, tachycardia may result in pulm edema
Need to rate control HR
High risk of afib (50-80%)
48
Q

Treatment of Mitral Stenosis (5)

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)
49
Q

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
? Increased risk of infectious endocarditis
No longer need prophylaxis when undergoing dental procedures.

50
Q

Mitral Regurgitation is caused by (4)

A

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

51
Q

Mitral Regurgitation Treatment (3)

A

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

52
Q

Acute Mitral Regurgitation (3)

A

Most common cause is Chordal Rupture
Also by MI, Endocarditis, Prosthetic Valve Dysfunction.
LA is not compliant and does not tolerate regurgitant flow well resulting in increased flow into the pulmonary circulation

53
Q

Mitral Valve Prolapse Causes

A
“Floppy” Valve
Most are female
Causes
Hyperadrenergic state
Connective tissue diseases
Ehlers-Danlos
Marfan
Chordae rupture
Characterized by mid-systolic clicks.
54
Q

Mitral Valve Prolapse

A

Beta blockers for hyperadrenergic state

Surgical repair

55
Q

Aortic Stenosis Most Common causes

A

Decreased flow from LV out to systemic system

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

Symptoms and Treatment of Aortic Stenosis

A
Characterized by
Systolic murmur in aortic area
Can cause severe symptoms (severely decreased forward flow)
Angina (decrease flow to endocardium)
Syncope
Hypotension
Treatment is surgery
Symptom treatment is treated with medication
Preload dependent
57
Q

Left Ventricular Outflow Tract Obstruction

A
Caused by 
Aortic Stenosis  
Supravalvular Stenosis
Subvalvular Stenosis
Hypertrophic Cardiomyopathy
Genetic Disorder
Severe Systemic HTN
Can cause systolic and/or Diastolic dysfunction
Preload Dependent
58
Q

Aortic Regurgitation

A

Historical number one cause is rheumatic heart disease
Now is congenital disease (bicuspid valve), endocarditis, HTN, Marfan, aortic dissection,
Characteristic
Diastolic murmur over aortic area
Most pts are aysmptomatic

59
Q

Treatment of 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
60
Q

Acute Aortic Regurgitation

A

The LV cannot compensate for the rapid filling during diastole which is caused by regurgitant blood.
Can be caused by
Endocarditis
Aortic Root Dissection
Complications of Prosthetic Valves
Spontaneous or traumatic rupture of the Valve

61
Q

Tricuspid Valve Stenosis

A

Usually as a result of valve repair, replacement or to carcinoid.
Not very common (now that rheumatic heart disease is rare)
R heart failure, hepatomegaly, ascites and edema common
Diastolic “rumble” that worsens with inspiration
Reduce fluid congestion
Valve replacement

62
Q

Tricuspid Regurgitation (5)

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

63
Q

Pulmonic Regurgitation (3)

A

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

64
Q

Acute Heart Failure

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

65
Q

First Way to Classify the Causes of Acute Heart Failure

A

1) Chronic cardiac conditions that predispose decompensation.
Systolic Dysfunction
Diastolic Dysfunction
Left Ventricular Outflow Tract Obstruction
Mitral Stenosis

66
Q

Second Way to Classify the Causes of Acute Heart Failure

A
2) Triggers that precipitate decompensation.
Myocardial ischemia/infection
Acute Aortic Regurgitation
Acute Mitral Regurgitation
Reno-vascular HTN
LA outflow impairment
Volume Overload
67
Q

Ischemic Heart Disease (3)

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