Congestive Heart Failure Part 1

Question 1

Epidemiology of Heart Failure

Answer 1

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)

Question 2

Causes of Heart Failure (4)

Answer 2

Ischemic Heart Disease 40%
Dilated Cardiomyopathy 32%
Primary Valvular Disease 12 %
Hypertensive Heart Disease 11%
Other 5%

Question 3

Developing Countries causes of HF (6)

Answer 3

Rheumatic Fever
Valvular 8%
Peripartum Cardiomyopathy
Idiopathic Cardiomyopathy 28%
Hypertension 33%
Ischemic Heart Disease 9%

Question 4

Action Potential

Answer 4

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.”

Question 5

Muscle Contraction

Answer 5

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

Question 6

Calcium in HF

Answer 6

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

Question 7

Normal Left Ventricular Pressure-Volume Relationship

Answer 7

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.

Question 8

Frank Starling relationship

Answer 8

EDV (preload) vs SV (CO + HR)

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

Question 9

Afterload

Answer 9

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.

Question 10

Contractility

Answer 10

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

Question 11

Definition of Heart Failure

Answer 11

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

Question 12

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

Answer 12

Systolic

Diastolic

Question 13

Systolic Dysfunction (2)

Answer 13

Decreased myocardial contractility.

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

Question 14

Issues with Systolic Dysfunction (5)

Answer 14

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)

Question 15

Diastolic Dysfunction

Answer 15

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

Question 16

Problems with Diastolic Dysfunction (7)

Answer 16

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)

Question 17

Neurohumoral Response (3)

Answer 17

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

Question 18

Different Pathways of Neurohumoral Response

Answer 18

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

Question 19

Complications of Neurohumoral Response (4)

Answer 19

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.

Question 20

Right Sided Heart Failure

Answer 20

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.

Question 21

Manifestations of Right Sided Heart Failure (8)

Answer 21

Slow and progressive unless PE
DOE
Fatigue
Syncope
Exertional angina
Anorexia
Hepatomegaly
JVD
Split S2

Question 22

Right Sided Failure Treatment (7)

Answer 22

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)

Question 23

Cardiomyopathy

Answer 23

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.”

Question 24

5 classes based on anatomy and physiology for Cardiomyopathy

Answer 24

Dilated
Hypertrophic
Restrictive
Arrhythmogenic Right Ventricular
Unclassified

Question 25

2 Types of Cardiomyopathy

Answer 25

Primary Genetic or acquired Secondary When other organ systems are involved

Question 26

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

Answer 26

``` Ischemic Valvular HTN Inflammatory Metabolic Toxic Genetic ```

Question 27

Dilated--Cardiomyopathy

Answer 27

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

Question 28

Causes of Dilated Cardiomyopathy (10)

Answer 28

``` 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% ```

Question 29

Hypertrophic Cardiomyopathy

Answer 29

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

Question 30

Hypertrophic Cardiomyopathy Epidemiology and Etiology

Answer 30

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

Question 31

Restrictive Cardiomyopathy (3)

Answer 31

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

Question 32

Restrictive Cardiomyopathy Classified as:

Answer 32

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)

Question 33

Arrhythmogenic Right Ventricular Cardiomyopathy

Answer 33

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

Question 34

Unclassified Cardiomyopathy (4)

Answer 34

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

Question 35

Takotsubo (stress-induced) Cardiomyopathy

Answer 35

``` “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 ```

Question 36

Peripartum Cardiomyopathy (4)

Answer 36

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

Question 37

Peripartum Cardiomyopathy 4 Criteria

Answer 37

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

Question 38

Risk Factors and Prognosis of Peripartum Cardiomyopathy

Answer 38

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%

Question 39

Alcoholic Cardiomyopathy

Answer 39

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

Question 40

Infectious Cardiomyopathy (8)

Answer 40

``` Viral Coxsackie Influenza Adenovirus Echovirus CMV HIV Chagas Disease Lyme Disease ```

Question 41

Toxic Cardiomyopathy (4)

Answer 41

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

Question 42

Valve

Answer 42

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.

Question 43

Function of Valve

Answer 43

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

Question 44

Mitral Stenosis Causes

Answer 44

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

Question 45

Mitral Stenosis

Answer 45

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

Question 46

2 Characteristic Findings on the Exam for Mitral Stenosis

Answer 46

Opening snap following S2 | Diastolic murmur loudest in mitral area

Question 47

Mild- Severe Mitral Stenosis

Answer 47

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%) ```

Question 48

Treatment of Mitral Stenosis (5)

Answer 48

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

Question 49

Mitral Regurgitation

Answer 49

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.

Question 50

Mitral Regurgitation is caused by (4)

Answer 50

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

Question 51

Mitral Regurgitation Treatment (3)

Answer 51

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

Question 52

Acute Mitral Regurgitation (3)

Answer 52

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

Question 53

Mitral Valve Prolapse Causes

Answer 53

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

Question 54

Mitral Valve Prolapse

Answer 54

Beta blockers for hyperadrenergic state | Surgical repair

Question 55

Aortic Stenosis Most Common causes

Answer 55

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 ```

Question 56

Symptoms and Treatment of Aortic Stenosis

Answer 56

``` 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 ```

Question 57

Left Ventricular Outflow Tract Obstruction

Answer 57

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

Question 58

Aortic Regurgitation

Answer 58

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

Question 59

Treatment of Aortic Regurgitation

Answer 59

``` 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 ```

Question 60

Acute Aortic Regurgitation

Answer 60

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

Question 61

Tricuspid Valve Stenosis

Answer 61

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

Question 62

Tricuspid Regurgitation (5)

Answer 62

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

Question 63

Pulmonic Regurgitation (3)

Answer 63

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

Question 64

Acute Heart Failure

Answer 64

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

Question 65

First Way to Classify the Causes of Acute Heart Failure

Answer 65

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

Question 66

Second Way to Classify the Causes of Acute Heart Failure

Answer 66

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

Question 67

Ischemic Heart Disease (3)

Answer 67

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